greenmedinfo--2020-06-30--Sweet basil extracts have an anti-inflammatory effect against adipocyte-induced inflammation.

Obesity , a lifestyle disease resulting from excessive caloric intake and insufficient physical activity , results in a state of chronic inflammation .
A food ingredient that suppresses chronic inflammation could help prevent associated diseases .
Sweet basil ( Ocimum basilicum L. ) is a herb from the Lamiaceae family with some reported anti-inflammatory effects .
Via this in vitro study , we aimed to investigate whether sweet basil exerts anti-inflammatory effects in obese patients .
Fresh sweet basil leaves were freeze-dried and powered .
After that , this was extracted with 80 % methanol .
After 3T3-L1 adipocytes were @ @ @ @ @ @ @ concentrations of either 5 or 25μg/mL for 24h , RAW264.7 macrophages were seeded onto this adipocytes and co-cultured for 12h .
We determined the effects of sweet basil extracts on inflammatory cytokine expression by real-time PCR or western blotting .
Sweet basil extracts reduced the expression of inflammatory cytokine mRNA inducedby co-culture , including that of IL-6 ( Il6 ) , IL-1β ( Il1b ) , TNF-α ( Tnf ) , and CCL2 ( Ccl2 ) .
In addition , sweet basil extracts suppressed the mRNA expression of NF-κB ( Nfκb1 ) , @ @ @ @ @ @ @ In an investigation of costimulatory CD137 ( Tnfrsf9 ) /CD137L inflammatorysignaling , a member of the TNF super-family , sweet basil extracts inhibited Tnfrsf9 expression induced by the co-culture .
Therefore , the results of this study indicated that sweet basil extracts have an anti-inflammatory effect against adipocyte-induced inflammation , possibly through suppression ofTnfrsf9 expression .

Obesity, a lifestyle disease resulting from excessive caloric intake and insufficient physical activity, results in a state of chronic inflammation. A food ingredient that suppresses chronic inflammation could help prevent associated diseases. Sweet basil (Ocimum basilicum L.) is a herb from the Lamiaceae family with some reported anti-inflammatory effects. Via this in vitro study, we aimed to investigate whether sweet basil exerts anti-inflammatory effects in obese patients. Fresh sweet basil leaves were freeze-dried and powered. After that, this was extracted with 80% methanol. After 3T3-L1 adipocytes were cultured with sweet basil extracts at final concentrations of either 5 or 25μg/mL for 24h, RAW264.7 macrophages were seeded onto this adipocytes and co-cultured for 12h. We determined the effects of sweet basil extracts on inflammatory cytokine expression by real-time PCR or western blotting. Sweet basil extracts reduced the expression of inflammatory cytokine mRNA inducedby co-culture, including that of IL-6 (Il6), IL-1β (Il1b), TNF-α (Tnf), and CCL2 (Ccl2). In addition, sweet basil extracts suppressed the mRNA expression of NF-κB (Nfκb1), a transcription factor of inflammatory cytokines. In an investigation of costimulatory CD137 (Tnfrsf9)/CD137L inflammatorysignaling, a member of the TNF super-family, sweet basil extracts inhibited Tnfrsf9 expression induced by the co-culture. Therefore, the results of this study indicated that sweet basil extracts have an anti-inflammatory effect against adipocyte-induced inflammation, possibly through suppression ofTnfrsf9 expression.


greenmedinfo--2020-06-30--Basil and sage essential oils are potentially highly efficient antipseudomonal agents.

The effects of basil ( Ocimum basilicum ) and sage ( Salvia officinalis ) essential oils on selected virulence factors @ @ @ @ @ biofilm resistance , motility , and pyocyanin production ) of Pseudomonas aeruginosa clinical isolates were @ @ @ @ @ for the first time .
The two essential oils were chemically characterized by GC and @ @ @ @ @ ( E ) -anethole were found to be the main components of the investigated basil @ @ @ @ @ were the major constituents of the studied sage essential oil .
The oils inhibited biofilm @ @ @ @ @ vs control , and significant reductions ( 74.7-99.9 % ) were also noted when the @ @ @ @ @ biofilms .
Likewise , swimming , swarming , and twitching motility patterns were highly affected @ @ @ @ @ basil and sage oils reduced pyocyanin production by 13.32-55.6 % and 5.0-58.7 % , respectively @ @ @ @ @ sage essential oils are potentially highly efficient antipseudomonal agents that could be used against both @ @ @ @ @

The effects of basil (Ocimum basilicum) and sage (Salvia officinalis) essential oils on selected virulence factors (biofilm formation, mature biofilm resistance, motility, and pyocyanin production) of Pseudomonas aeruginosa clinical isolates were evaluated in the present study for the first time. The two essential oils were chemically characterized by GC and GC-MS analyses. Linalool and (E)-anethole were found to be the main components of the investigated basil oil, whileα-thujone and camphor were the major constituents of the studied sage essential oil. The oils inhibited biofilm formation up to 99.9% vs control, and significant reductions (74.7-99.9%) were also noted when the oils were applied to mature biofilms. Likewise, swimming, swarming, and twitching motility patterns were highly affected by both oils. The basil and sage oils reduced pyocyanin production by 13.32-55.6% and 5.0-58.7%, respectively. Thus, basil and sage essential oils are potentially highly efficient antipseudomonal agents that could be used against both acute and chronic infections.


greenmedinfo--2020-06-30--Physiological and histopathological study on the influence of Ocimum basilicum leaves extract on thi

Physiological and histopathological study on the influence of Ocimum basilicum leaves extract on thioacetamide-induced nephrotoxicity.

Kidney disease is a worldwide public health problem that affects millions of people worldwide .
Globally , many risk factors for kidney disease progression have been identified .
The global prevalence of acute and chronic forms of kidney disease is rising continuously .
Nephrotoxicity is defined as rapid dysfunction of kidney due to toxic influence of medications and chemicals .
Nephroprotective agents are material that has potential to minimize the effects of nephrotoxic agents .
Plants have been shown to be potential therapeutic agents to protect against nephrotoxicity .
The purpose of the present study was to evaluate the nephroprotective @ @ @ @ @ @ @ ( TAA ) in male rats .
Experimental male rats were divided into four groups .
Rats of the first group were served as controls .
Rats of the second group were exposed to TAA .
Rats of the third group were treated with basil leaves extract and TAA .
Rats of the fourth group were treated with basil leaves extract .
After the end of experimental duration ( 6 Weeks ) , rats of the second group showed significantly increases of serum creatinine , blood urea nitrogen and uric acid levels , @ @ @ @ @ @ @ and glutathione were significantly decreased .
Histopathologically , renal sections from rats treated with only TAA showed several alterations in the structure of most renal corpuscles including a degeneration of glomeruli and Bowman 's capsules .
Treatment with basil leaves extract improved the observed biochemical and histopathological changes induced by TAA intoxication .
These new findings indicate that the extract of basil leaves represent protective roles on biochemical and histopathological changes induced by TAA toxicity due to its antioxidant activities .

Kidney disease is a worldwide public health problem that affects millions of people worldwide. Globally, many risk factors for kidney disease progression have been identified. The global prevalence of acute and chronic forms of kidney disease is rising continuously. Nephrotoxicity is defined as rapid dysfunction of kidney due to toxic influence of medications and chemicals. Nephroprotective agents are material that has potential to minimize the effects of nephrotoxic agents. Plants have been shown to be potential therapeutic agents to protect against nephrotoxicity. The purpose of the present study was to evaluate the nephroprotective effect of basil leaves extract against thioacetamide (TAA) in male rats. Experimental male rats were divided into four groups. Rats of the first group were served as controls. Rats of the second group were exposed to TAA. Rats of the third group were treated with basil leaves extract and TAA. Rats of the fourth group were treated with basil leaves extract. After the end of experimental duration (6 Weeks), rats of the second group showed significantly increases of serum creatinine, blood urea nitrogen and uric acid levels, while the levels of serum superoxide dismutase and glutathione were significantly decreased. Histopathologically, renal sections from rats treated with only TAA showed several alterations in the structure of most renal corpuscles including a degeneration of glomeruli and Bowman's capsules. Treatment with basil leaves extract improved the observed biochemical and histopathological changes induced by TAA intoxication. These new findings indicate that the extract of basil leaves represent protective roles on biochemical and histopathological changes induced by TAA toxicity due to its antioxidant activities.


greenmedinfo--2020-06-30--Thyme, basil and marjoram essential oils have synergistic antimicrobial action against Escherichia c

Thyme, basil and marjoram essential oils have synergistic antimicrobial action against Escherichia coli and Staphylococcus aureus.

To replace synthetic preservatives and expand green consumption , several essential oils have been tested in foods and food packaging @ @ @ @ @ .
This study aimed to analyze the synergistic antimicrobial action of a chitosan-gelatin based active @ @ @ @ @ essential oils ( EOs ) .
The antimicrobial agents were tested against foodborne microorganisms Staphylococcus @ @ @ @ @ .
The antibacterial activity of Thymus vulgaris , Ocimum basilicum , Origanum majorana , and @ @ @ @ @ were assessed according to the minimum inhibitory concentration ( MIC ) and minimum bactericidal concentration @ @ @ @ @ microdilution method .
Chitosan-gelatin based active biopolymers were developed , and 23 % ( w/w @ @ @ @ @ and combined oils were added .
The antimicrobial effect of active films was measured using @ @ @ @ @ Active films with the addition of essential oils have potential applications as active packaging agents @ @ @ @ @ inhibition zones .
Combined EOs can be used to enhance the antimicrobial activity , ensuring @ @ @ @ @ packaging and decreasing the association with adverse sensory characteristics .

To replace synthetic preservatives and expand green consumption, several essential oils have been tested in foods and food packaging due to their antimicrobial properties. This study aimed to analyze the synergistic antimicrobial action of a chitosan-gelatin based active biopolymers with the addition of essential oils (EOs). The antimicrobial agents were tested against foodborne microorganisms Staphylococcus aureus and Escherichia coli strains. The antibacterial activity of Thymus vulgaris, Ocimum basilicum, Origanum majorana, and the synergistic interactions among them were assessed according to the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) using the microdilution method. Chitosan-gelatin based active biopolymers were developed, and 23% (w/w) of each essential oil and combined oils were added. The antimicrobial effect of active films was measured using the disk diffusion method. Active films with the addition of essential oils have potential applications as active packaging agents, especially those that demonstrated inhibition zones. Combined EOs can be used to enhance the antimicrobial activity, ensuring reduced doses used in active packaging and decreasing the association with adverse sensory characteristics.


greenmedinfo--2020-06-30--Combination of luteolin and lycopene effectively protect against nonalcoholic fatty liver disease.

AIM : Luteolin and lycopene are common natural products , widely existing in nature , and both of which were reported to have various biological functions including anti-inflammatory , anti-obesity and anti-NAFLD .
In the present study , we aimed to evaluate the therapeutic efficacy of luteolin and lycopene in combination and its latent molecular mechanisms in vitro and in vivo models of NAFLD .
MAIN METHODS : Sodium palmitate ( PA ) -induced steatotic HepG2 cells and primary hepatocytes , and high-fat diet-induced C57BL/6J obese mice were treated with luteolin , lycopene and their combination .
Metabolic parameters were @ @ @ @ @ @ @ that luteolin ( 20 μM ) + lycopene ( 10 μM ) was the best therapeutic combination in PA-induced HepG2 cells , and significantly improve cell viability and lipid accumulation in PA-induced HepG2 cells and primary hepatocytes .
In addition , luteolin ( 20 mg/kg ) + lycopene ( 20 mg/kg ) could ameliorate increased bodyweight and hepatocyte steatosis ; regulate serum triglycerides , serum total cholesterol , hepatic triglycerides and hepatic total cholesterol ; decrease serum alanine transaminase and aspartate transaminase .
Furthermore , in vivo and in vitro , luteolin , @ @ @ @ @ @ @ on Sirt1 expression , but all of them could upregulate the expression of NAMPT , which could increase the level of NAD+ , the co-substrate of Sirt1 , indirectly activating Sirt1/AMPK pathway , and then inhibited lipogenesis and increased β-oxidation , defensing the '' first hit '' ; they also inactivated nuclear factor-κB ( NF-κB ) and decreased the levels of IL-6 , IL-1β and TNF-α , defensing the '' second hit '' .
SIGNIFICANCE : Thus , luteolin and lycopene in combination can effectively ameliorate '' two-hit '' in NAFLD through activation @ @ @ @ @

AIM: Luteolin and lycopene are common natural products, widely existing in nature, and both of which were reported to have various biological functions including anti-inflammatory, anti-obesity and anti-NAFLD. In the present study, we aimed to evaluate the therapeutic efficacy of luteolin and lycopene in combination and its latent molecular mechanisms in vitro and in vivo models of NAFLD.
MAIN METHODS: Sodium palmitate (PA)-induced steatotic HepG2 cells and primary hepatocytes, and high-fat diet-induced C57BL/6J obese mice were treated with luteolin, lycopene and their combination. Metabolic parameters were measured.
KEY FINDINGS: We found that luteolin (20 μM) + lycopene (10 μM) was the best therapeutic combination in PA-induced HepG2 cells, and significantly improve cell viability and lipid accumulation in PA-induced HepG2 cells and primary hepatocytes. In addition, luteolin (20 mg/kg) + lycopene (20 mg/kg) could ameliorate increased bodyweight and hepatocyte steatosis; regulate serum triglycerides, serum total cholesterol, hepatic triglycerides and hepatic total cholesterol; decrease serum alanine transaminase and aspartate transaminase. Furthermore, in vivo and in vitro, luteolin, lycopene and their combination had no effect on Sirt1 expression, but all of them could upregulate the expression of NAMPT, which could increase the level of NAD+, the co-substrate of Sirt1, indirectly activating Sirt1/AMPK pathway, and then inhibited lipogenesis and increased β-oxidation, defensing the"first hit"; they also inactivated nuclear factor-κB (NF-κB) and decreased the levels of IL-6, IL-1β and TNF-α, defensing the"second hit".
SIGNIFICANCE: Thus, luteolin and lycopene in combination can effectively ameliorate"two-hit"in NAFLD through activation of the Sirt1/AMPK pathway.


greenmedinfo--2020-06-30--Luteolin reduces fluid hypersecretion by inhibiting TMEM16A in interleukin-4 treated calu-3 airway e

Luteolin reduces fluid hypersecretion by inhibiting TMEM16A in interleukin-4 treated calu-3 airway epithelial cells.

Rhinorrhea in allergic rhinitis ( AR ) is characterized by the secretion of electrolytes in the nasal discharge .
The secretion of Cland HCOis mainly regulated by cystic fibrosis transmembrane conductance regulator ( CFTR ) or via the calciumactivated Clchannel anoctamin-1 ( ANO1 ) in nasal gland serous cells .
Interleukin-4 ( IL-4 ) , which is crucial in the development of allergic inflammation , increases the expression and activity of ANO1 by stimulating histamine receptors .
In this study , we investigated ANO1 as a potential therapeutic target for rhinorrhea in AR using an ANO1 inhibitor derived from a @ @ @ @ @ @ @ % ) of ( SP ) and its five major flavonoids constituents were prepared .
To elucidate whether the activity of human ANO1 ( hANO1 ) was modulated by SPand its chemical constituents , a patch clamp experiment was performed in hANO1-HEK293T cells .
Luteolin , one of the major chemical constituents in SP , significantly inhibited hANO1 activity in hANO1-HEK293T cells .
Further , SPand luteolin specifically inhibited the calcium-activated chloride current , but not CFTR current in human airway epithelial Calu-3 cells .
Calu-3 cells were cultured to confluency on transwell @ @ @ @ @ @ @ measure the electrolyte transport by Ussing chamber .
Luteolin also significantly inhibited the ATP-induced increase in electrolyte transport , which was increased in IL-4 sensitized Calu-3 cells .
Our findings indicate that SPand luteolin may be suitable candidates for the prevention and treatment of allergic rhinitis .
SPEtOH- and luteolin-mediated ANO1 regulation provides a basis for the development of novel approaches for the treatment of allergic rhinitis-induced rhinorrhea .

Rhinorrhea in allergic rhinitis (AR) is characterized by the secretion of electrolytes in the nasal discharge. The secretion of Cland HCOis mainly regulated by cystic fibrosis transmembrane conductance regulator (CFTR) or via the calciumactivated Clchannel anoctamin-1 (ANO1) in nasal gland serous cells. Interleukin-4 (IL-4), which is crucial in the development of allergic inflammation, increases the expression and activity of ANO1 by stimulating histamine receptors. In this study, we investigated ANO1 as a potential therapeutic target for rhinorrhea in AR using an ANO1 inhibitor derived from a natural herb. Ethanolic extracts (30%) of(SP) and its five major flavonoids constituents were prepared. To elucidate whether the activity of human ANO1 (hANO1) was modulated by SPand its chemical constituents, a patch clamp experiment was performed in hANO1-HEK293T cells. Luteolin, one of the major chemical constituents in SP, significantly inhibited hANO1 activity in hANO1-HEK293T cells. Further, SPand luteolin specifically inhibited the calcium-activated chloride current, but not CFTR current in human airway epithelial Calu-3 cells. Calu-3 cells were cultured to confluency on transwell inserts in the presence of IL-4 to measure the electrolyte transport by Ussing chamber. Luteolin also significantly inhibited the ATP-induced increase in electrolyte transport, which was increased in IL-4 sensitized Calu-3 cells. Our findings indicate that SPand luteolin may be suitable candidates for the prevention and treatment of allergic rhinitis. SPEtOH- and luteolin-mediated ANO1 regulation provides a basis for the development of novel approaches for the treatment of allergic rhinitis-induced rhinorrhea.


greenmedinfo--2020-06-30--Luteolin is expounded to have great potential to target various genes and pathways to perform anti-i

Luteolin is expounded to have great potential to target various genes and pathways to perform anti-inflammatory effects.

Luteolin , a natural flavonoid exists in various medicinal plants , has strong anti-inflammatory effect .
However , anti-inflammatory mechanism of luteolin has not been fully explored .
Hence , we systematically investigated druggability and anti-inflammatory mechanism of luteolin based on network pharmacology and in vitro experiments .
The absorption , distribution , metabolism and excretion of luteolin were evaluated by TCMSP server .
Targets associated with luteolin and inflammation were collected from public databases , and the overlapping targets between luteolin and inflammation were analyzed by Draw Venn diagram .
Then the protein-protein interaction network of luteolin against inflammation @ @ @ @ @ @ @ and pathway enrichment analysis were performed .
Finally , in vitro experiments were carried out to estimate the accuracy of predicted target genes .
ADME results indicated that luteolin has great potential to be developed into a drug .
226 overlapping targets were screened by matching 280 targets of luteolin with 9015 targets of inflammation .
9 core targets of luteolin against inflammation were identified , including MMP9 , MAPK1 , HSP90AA1 , CASP3 , ALB , EGFR , SRC , HRAS and ESR1 .
Gene function were mainly involved in metabolism , @ @ @ @ @ @ @ pathways , pathways in cancer , PI3K-AKT signaling pathway , Ras signaling pathway and so on might be the critical pathways of luteolin against inflammation .
RT-qPCR and ELISA results indicated that luteolin decreased the expression of most of core genes at protein and mRNA levels ( MMP9 , MAPK1 , HSP90AA1 , EGFR , SRC and HRAS ) .
Luteolin is expounded to have great potential to be developed into a drug and target various genes and pathways to perform anti-inflammatory effect .

Luteolin, a natural flavonoid exists in various medicinal plants, has strong anti-inflammatory effect. However, anti-inflammatory mechanism of luteolin has not been fully explored. Hence, we systematically investigated druggability and anti-inflammatory mechanism of luteolin based on network pharmacology and in vitro experiments. The absorption, distribution, metabolism and excretion of luteolin were evaluated by TCMSP server. Targets associated with luteolin and inflammation were collected from public databases, and the overlapping targets between luteolin and inflammation were analyzed by Draw Venn diagram. Then the protein-protein interaction network of luteolin against inflammation was constructed. Further, gene function and pathway enrichment analysis were performed. Finally, in vitro experiments were carried out to estimate the accuracy of predicted target genes. ADME results indicated that luteolin has great potential to be developed into a drug. 226 overlapping targets were screened by matching 280 targets of luteolin with 9015 targets of inflammation. 9 core targets of luteolin against inflammation were identified, including MMP9, MAPK1, HSP90AA1, CASP3, ALB, EGFR, SRC, HRAS and ESR1. Gene function were mainly involved in metabolism, energy pathways and signal transduction. Metabolic pathways, pathways in cancer, PI3K-AKT signaling pathway, Ras signaling pathway and so on might be the critical pathways of luteolin against inflammation. RT-qPCR and ELISA results indicated that luteolin decreased the expression of most of core genes at protein and mRNA levels (MMP9, MAPK1, HSP90AA1, EGFR, SRC and HRAS). Luteolin is expounded to have great potential to be developed into a drug and target various genes and pathways to perform anti-inflammatory effect.


greenmedinfo--2020-06-30--Luteolin improves hypercholesterolemia and glucose intolerance.

Luteolin , a naturally derived flavonoid , exerts beneficial effects such as antitumor , antioxidant , and anti-inflammatory effects .
However , the molecular mechanism underlying the effect of luteolin in hypercholesterolemia remains unclear .
In this study , we demonstrated that luteolin upregulated the expression of liver X receptor ( LXR ) α , ATP-binding cassette transporter G1 ( ABCG1 ) , and scavenger receptor class B member 1 ( SRB1 ) , which play a major role in cholesterol efflux , in HepG2 hepatocytes .
Luteolin-stimulated expression of ABCG1 and SRB1 was reversed by inhibitory compound of LXRα @ @ @ @ @ @ @ of ABCG1 , and SRB1 as well as cholesterol 7 α-hydroxylase ( Cyp7α1 ) in the liver of diet-induced obese mice .
Luteolin decreased the level of blood cholesterol and non-high-density lipoprotein cholesterol in obese mice .
In addition , luteolin ameliorated glucose intolerance and reduced expression of gluconeogenesis-associated enzymes in an LXRα-dependent manner .
PRACTICAL APPLICATIONS : Luteolin is known to possess various pharmacological activities .
This research revealed that luteolin ameliorates hypercholesterolemia and glucose intolerance in diet-induced obesity .
The results indicate that the potential properties of luteolin in cholesterol metabolism @ @ @ @ @ @ @ part , as being due to upregulated expression of ABCG1 , and SRB1 through activation of liver X receptor , LXRα signaling pathway in HepG2 cells .

Luteolin, a naturally derived flavonoid, exerts beneficial effects such as antitumor, antioxidant, and anti-inflammatory effects. However, the molecular mechanism underlying the effect of luteolin in hypercholesterolemia remains unclear. In this study, we demonstrated that luteolin upregulated the expression of liver X receptor (LXR)α, ATP-binding cassette transporter G1 (ABCG1), and scavenger receptor class B member 1 (SRB1), which play a major role in cholesterol efflux, in HepG2 hepatocytes. Luteolin-stimulated expression of ABCG1 and SRB1 was reversed by inhibitory compound of LXRα. Luteolin administration also upregulated the expression of ABCG1, and SRB1 as well as cholesterol 7 α-hydroxylase (Cyp7α1) in the liver of diet-induced obese mice. Luteolin decreased the level of blood cholesterol and non-high-density lipoprotein cholesterol in obese mice. In addition, luteolin ameliorated glucose intolerance and reduced expression of gluconeogenesis-associated enzymes in an LXRα-dependent manner. PRACTICAL APPLICATIONS: Luteolin is known to possess various pharmacological activities. This research revealed that luteolin ameliorates hypercholesterolemia and glucose intolerance in diet-induced obesity. The results indicate that the potential properties of luteolin in cholesterol metabolism could be explained, at least in part, as being due to upregulated expression of ABCG1, and SRB1 through activation of liver X receptor, LXRα signaling pathway in HepG2 cells.


greenmedinfo--2020-07-01--The cancer chemopreventive and therapeutic potential of tetrahydrocurcumin.

In recent decades , cancer has been one of the leading causes of death worldwide .
Despite advances in understanding the molecular basis of tumorigenesis , diagnosis , and clinical therapies , the discovery and development of effective drugs is an active and vital field in cancer research .
Tetrahydrocurcumin is a major curcuminoid metabolite of curcumin , naturally occurring in turmeric .
The interest in tetrahydrocurcumin research is increasing because it is superior to curcumin in its solubility in water , chemical stability , bioavailability , and anti-oxidative activity .
Many in vitro and in vivo studies have revealed @ @ @ @ @ @ @ mechanisms , including modulation of oxidative stress , xenobiotic detoxification , inflammation , proliferation , metastasis , programmed cell death , and immunity .
Despite the pharmacological similarities between tetrahydrocurcumin and curcumin , the structure of tetrahydrocurcumin determines its distinct and specific molecular mechanism , thus making it a potential candidate for the prevention and treatment of cancers .
However , the utility of tetrahydrocurcumin is yet to be evaluated as only limited pharmacokinetic and oral bioavailability studies have been performed .
This review summarizes research on the anti-cancer properties of tetrahydrocurcumin and @ @ @ @ @ @

In recent decades, cancer has been one of the leading causes of death worldwide. Despite advances in understanding the molecular basis of tumorigenesis, diagnosis, and clinical therapies, the discovery and development of effective drugs is an active and vital field in cancer research. Tetrahydrocurcumin is a major curcuminoid metabolite of curcumin, naturally occurring in turmeric. The interest in tetrahydrocurcumin research is increasing because it is superior to curcumin in its solubility in water, chemical stability, bioavailability, and anti-oxidative activity. Many in vitro and in vivo studies have revealed that tetrahydrocurcumin exerts anti-cancer effects through various mechanisms, including modulation of oxidative stress, xenobiotic detoxification, inflammation, proliferation, metastasis, programmed cell death, and immunity. Despite the pharmacological similarities between tetrahydrocurcumin and curcumin, the structure of tetrahydrocurcumin determines its distinct and specific molecular mechanism, thus making it a potential candidate for the prevention and treatment of cancers. However, the utility of tetrahydrocurcumin is yet to be evaluated as only limited pharmacokinetic and oral bioavailability studies have been performed. This review summarizes research on the anti-cancer properties of tetrahydrocurcumin and describes its mechanisms of action.


greenmedinfo--2020-07-01--Top Five Health Benefits of Ginsenosides

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greenmedinfo--2020-07-01--Tetrahydrocurcumin ameliorates diabetes profiles of db/db mice.

Diabetes is a worldwide healthy concern , which affects approximately 9 % of the population .
Tetrahydrocurcumin ( THC ) is the main metabolite of curcumin , which exerts the anti-diabetic activity .
However , the underlying mechanism has not been clarified .
In the research , we investigated whether THC could improve diabetes by regulating the gut microbiota and the expression of pancreatic glucagon-like peptide-1 ( GLP-1 ) in the db/db mice .
After 8-week THC administration ( ig.
, once a day , THCH group : 200 mg/kg , THCL group : 100 mg/kg ) , the fasting @ @ @ @ @ @ @ every two weeks .
Serum insulin levels , the expression of GLP-1 in the pancreas , the histopathology of pancreas and the composition of gut microbiota were evaluated at the end of the experiment .
Compared to the diabetic group , THC treatment decreased significantly blood glucose , increased the secretion of insulin and the expression of GLP-1 in the pancreas .
Histomorphological analysis revealed that THC could protect pancreatic islet cells against hyperglycemic insult .
Furthermore , the data from the sequencing of the16S rDNA genes in gut microbiome displayed that THC @ @ @ @ @ @ @ the lowered relative abundance of Proteobacteria , Actinobacteria and the ratio of Firmicutes to Bacteroidetes .
The linear regression analysis showed a close correlation between the GLP-1 expressionand the proportion of the intestinal microflora .
Altogether , these results demonstrated that THC might have a direct regulatory effect on gut microflora , which indirectly decrease the FBG levels by modulating GLP-1 expression in the pancreas .

Diabetes is a worldwide healthy concern, which affects approximately 9% of the population. Tetrahydrocurcumin (THC) is the main metabolite of curcumin, which exerts the anti-diabetic activity. However, the underlying mechanism has not been clarified. In the research, we investigated whether THC could improve diabetes by regulating the gut microbiota and the expression of pancreatic glucagon-like peptide-1 (GLP-1) in the db/db mice. After 8-week THC administration (ig., once a day, THCH group: 200 mg/kg, THCL group: 100 mg/kg), the fasting blood glucose (FBG) was measured every two weeks. Serum insulin levels, the expression of GLP-1 in the pancreas, the histopathology of pancreas and the composition of gut microbiota were evaluated at the end of the experiment. Compared to the diabetic group, THC treatment decreased significantly blood glucose, increased the secretion of insulin and the expression of GLP-1 in the pancreas. Histomorphological analysis revealed that THC could protect pancreatic islet cells against hyperglycemic insult. Furthermore, the data from the sequencing of the16S rDNA genes in gut microbiome displayed that THC could restore the intestinal dysbiosis, including the lowered relative abundance of Proteobacteria, Actinobacteria and the ratio of Firmicutes to Bacteroidetes. The linear regression analysis showed a close correlation between the GLP-1 expressionand the proportion of the intestinal microflora. Altogether, these results demonstrated that THC might have a direct regulatory effect on gut microflora, which indirectly decrease the FBG levels by modulating GLP-1 expression in the pancreas.


greenmedinfo--2020-07-01--Tetrahydrocurcumin mitigates acute hypobaric hypoxia-induced cerebral oedema and inflammation.

High-altitude cerebral oedema ( HACE ) is a potentially fatal manifestation of high-altitude sickness and is caused partly by inflammation and the blood-brain barrier disruption .
Tetrahydrocurcumin ( THC ) has been reported to exert effective antioxidative and anti-inflammatory effects ; This study sought to elucidate the underlying mechanism of THC in mitigating HACE using a mouse model .
Our results revealed that prophylactic administration of THC ( 40 mg/kg ) for 3 days significantly alleviated the increase in brain water content ( BWC ) , interleukin-1β ( IL-1β ) and TNF-α levels caused by acute hypobaric hypoxia ( AHH @ @ @ @ @ @ @ SOD ) activity was increased by THC to enhance the ability to resist hypoxia .
Histologicaland ultrastructural analysis of the cerebrum revealed that THC administration mitigated AHH-induced pericellular oedema and reduced the perivascular space , resulting in the simultaneous remission of oedema and protection of mitochondria in the cerebrum .
In vitro , astrocytes exposed to hypoxia ( 4 % O ) for 24 hr exhibited and increase in IL-1β expression followed by an increase in vascular endothelial growth factor ( VEGF ) levels .
Furthermore , THC administration remarkably downregulated VEGF , @ @ @ @ @ @ @ nuclear factor kappa-light-chain-enhancer of activated B cells ( NF-κB ) expression , both in vivo and in vitro .
Our data highlight the potential prophylactic activity of THC in HACE , it effectively mitigates AHH-induced cerebral oedema and inflammation is associated with the inhibition of the NF-κB/ VEGF/MMP-9 pathways .

High-altitude cerebral oedema (HACE) is a potentially fatal manifestation of high-altitude sickness and is caused partly by inflammation and the blood-brain barrier disruption. Tetrahydrocurcumin (THC) has been reported to exert effective antioxidative and anti-inflammatory effects; This study sought to elucidate the underlying mechanism of THC in mitigating HACE using a mouse model. Our results revealed that prophylactic administration of THC (40 mg/kg) for 3 days significantly alleviated the increase in brain water content (BWC), interleukin-1β (IL-1β) and TNF-α levels caused by acute hypobaric hypoxia (AHH). Additionally, superoxide dismutase (SOD) activity was increased by THC to enhance the ability to resist hypoxia. Histologicaland ultrastructural analysis of the cerebrum revealed that THC administration mitigated AHH-induced pericellular oedema and reduced the perivascular space, resulting in the simultaneous remission of oedema and protection of mitochondria in the cerebrum. In vitro, astrocytes exposed to hypoxia (4% O) for 24 hr exhibited and increase in IL-1β expression followed by an increase in vascular endothelial growth factor (VEGF) levels. Furthermore, THC administration remarkably downregulated VEGF, matrix metallopeptidase-9 (MMP-9), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)expression, both in vivo and in vitro. Our data highlight the potential prophylactic activity of THC in HACE, it effectively mitigates AHH-induced cerebral oedema and inflammation is associated with the inhibition of the NF-κB/ VEGF/MMP-9 pathways.


greenmedinfo--2020-07-01--Bisdemethoxycurcumin exerts a cell-protective effect via JAK2/STAT3 signalling in a rotenone-induced

Bisdemethoxycurcumin exerts a cell-protective effect via JAK2/STAT3 signalling in a rotenone-induced Parkinson's disease model in vitro.

INTRODUCTION : Oxidative stress and cell apoptosis have both been suggested to be closely associated with the pathogenesis of Parkinson 's disease ( PD ) .
Previously , bisdemethoxycurcumin ( BDMC ) has been shown to exhibit several desirable characteristics as a candidate neuroprotective agent , including antioxidant and anti-inflammatory activities in the nervous system .
However , whether BDMC can exert cell-protective roles in an in vitro model of PD remains unknown .
MATERIAL AND METHODS : SH-SY5Y cells were pretreated with BDMC , with or without AG490 and SI-201 , for 30 min , followed by a co-incubation @ @ @ @ @ @ @ a cell viability assay and western blotting was performed , and SOD and GSH activities were analyzed .
RESULTS : The results revealed that the pretreatment with BDMC enhanced the cell survival , antioxidative stress capacity and the phosphorylation levels of JAK/STAT3 in SH-SY5Y cells treated with rotenone .
However , following the incubation with AG490 and SI-201 , inhibitors of the JAK/STAT3 signaling pathway , BDMC was unable to exert cell-protective roles in SH-SY5Y cells treated with rotenone .
CONCLUSIONS : In conclusion , the results suggested that BDMC may exert a @ @ @ @ @ @ @ via JAK2/STAT3 signaling , thus suggesting the possible application of BDMC for the treatment of neurodegenerative diseases related to JAK2/STAT3 signaling .

INTRODUCTION: Oxidative stress and cell apoptosis have both been suggested to be closely associated with the pathogenesis of Parkinson's disease (PD). Previously, bisdemethoxycurcumin (BDMC) has been shown to exhibit several desirable characteristics as a candidate neuroprotective agent, including antioxidant and anti-inflammatory activities in the nervous system. However, whether BDMC can exert cell-protective roles in an in vitro model of PD remains unknown.
MATERIAL AND METHODS: SH-SY5Y cells were pretreated with BDMC, with or without AG490 and SI-201, for 30 min, followed by a co-incubation with rotenone for 24 h. Subsequently, a cell viability assay and western blotting was performed, and SOD and GSH activities were analyzed.
RESULTS: The results revealed that the pretreatment with BDMC enhanced the cell survival, antioxidative stress capacity and the phosphorylation levels of JAK/STAT3 in SH-SY5Y cells treated with rotenone. However, following the incubation with AG490 and SI-201, inhibitors of the JAK/STAT3 signaling pathway, BDMC was unable to exert cell-protective roles in SH-SY5Y cells treated with rotenone.
CONCLUSIONS: In conclusion, the results suggested that BDMC may exert a cell-protective role in SH-SY5Y cells in vitro via JAK2/STAT3 signaling, thus suggesting the possible application of BDMC for the treatment of neurodegenerative diseases related to JAK2/STAT3 signaling.


greenmedinfo--2020-07-01--Protective effects of maternal administration of curcumin and hesperidin in the rat offspring follow

Protective effects of maternal administration of curcumin and hesperidin in the rat offspring following repeated febrile seizure.

Neuroinflammation has a key role in seizure generation and perpetuation in the neonatal period , and toll-like receptor 4 ( TLR4 ) pathway has a prominent role in neuroinflammatory diseases .
Administration of antioxidants and targeting TLR4 in the embryonic period may protect rat offspring against the next incidence of febrile seizure and its harmful effects .
Curcumin and hesperidin are natural compounds with anti-inflammatory and antioxidant properties and have an inhibitory action on TLR4 receptors .
We evaluated the effect of maternal administration of curcumin and hesperidin on infantile febrile seizure and subsequent memory dysfunction in adulthood .
Hyperthermia @ @ @ @ @ @ @ 9-11 on male rat pups with 24 h intervals , in a Plexiglas box that was heated to ~45 °C by a heat lamp .
We used enzyme-linked immunosorbent assay , Western blotting , malondialdehyde ( MDA ) , and glutathione ( GSH ) assessment for evaluation of inflammatory cytokine levels , TLR4 protein expression , and oxidative responses in the hippocampal tissues .
For assessing working memory and long-term potentiation , the double Y-maze test and Schaffer collateral-CA1 in vivo electrophysiological recording were performed , respectively Our results showed that curcumin and @ @ @ @ @ @ @ TLR4 protein expression andreversed memory dysfunction .
However , they did not provoke a significant effect on GSH content or amplitude and slope of recorded fEPSPs in the hippocampus .
In addition , curcumin , but not hesperidin , decreased interleukin-1β ( IL-1β ) and MDA levels .
These findings imply that curcumin and hesperidin induced significant protective effects on febrile seizures , possibly via their anti-inflammatory and antioxidant properties and downregulation of TLR4 .

Neuroinflammation has a key role in seizure generation and perpetuation in the neonatal period, and toll-like receptor 4 (TLR4) pathway has a prominent role in neuroinflammatory diseases. Administration of antioxidants and targeting TLR4 in the embryonic period may protect rat offspring against the next incidence of febrile seizure and its harmful effects. Curcumin and hesperidin are natural compounds with anti-inflammatory and antioxidant properties and have an inhibitory action on TLR4 receptors. We evaluated the effect of maternal administration of curcumin and hesperidin on infantile febrile seizure and subsequent memory dysfunction in adulthood. Hyperthermia febrile seizure was induced on postnatal days 9-11 on male rat pups with 24 h intervals, in a Plexiglas box that was heated to ~45 °C by a heat lamp. We used enzyme-linked immunosorbent assay, Western blotting, malondialdehyde (MDA), and glutathione (GSH) assessment for evaluation of inflammatory cytokine levels, TLR4 protein expression, and oxidative responses in the hippocampal tissues. For assessing working memory and long-term potentiation, the double Y-maze test and Schaffer collateral-CA1 in vivo electrophysiological recording were performed, respectively Our results showed that curcumin and hesperidin decreased TNF-α, IL-10, and TLR4 protein expression andreversed memory dysfunction. However, they did not provoke a significant effect on GSH content or amplitude and slope of recorded fEPSPs in the hippocampus. In addition, curcumin, but not hesperidin, decreased interleukin-1β (IL-1β) and MDA levels. These findings imply that curcumin and hesperidin induced significant protective effects on febrile seizures, possibly via their anti-inflammatory and antioxidant properties and downregulation of TLR4.


greenmedinfo--2020-07-01--Co-administration of flaxseed and hesperidin appears to be superior to either supplementation alone

Co-administration of flaxseed and hesperidin appears to be superior to either supplementation alone on metabolic syndrome treatment.

PURPOSE : The aim of the present study was to compare the clinical effect of flaxseed and hesperidin alone and with combination in patients with metabolic syndrome .
Number of participants with treated metabolic syndrome was assessed as a primary end point .
METHODS : In this 12-week randomized controlled trial , ninety-eight patients with metabolic syndrome randomly assigned to receive either whole flaxseed powder ( 30 g/day ) , or hesperidin ( 1 g/day ) , or combination of 30 g flaxseed and 1 g hesperidin or no supplement while adhering a lifestyle modification program .
RESULTS : In @ @ @ @ @ @ @ pressure ( - 5.68 vs. - 2.91 mmHg , P = 0.041 ) and serum concentrations of triglyceride ( - 50.06 vs. 3.87 mg/dL , P = 0.033 ) in hesperidin group showed a significant reduction over 12 weeks of intervention .
Comparison of the results of flaxseed group with the control group showed a significant improvement in serum concentrations of triglyceride ( - 66 vs. 3.87 mg/dL , P = 0.028 ) , insulin ( - 4.27 vs. - 2.51 mU/L , P = 0.003 ) and accordingly insulin resistance ( - @ @ @ @ @ @ @ 0.005 ) and sensitivity ( 0.03 vs. 0.01 , P = 0.022 ) indices in flaxseed group .
Combination of flaxseed and hesperidin improved three of five metabolic syndrome components including serum concentrations of triglyceride , glucose and systolic blood pressure as compared to placebo .
Interestingly , co-administration of flaxseed and hesperidin with 77.3 % reduction in the prevalence of defined metabolic syndrome was revealed to be most effective in controlling the metabolic syndrome , after which the group of flaxseed with 76 % reduction and hesperidin group with 54.5 % reduction @ @ @ @ @ @ @ .
CONCLUSIONS : It can be concluded that co-administration of flaxseed and hesperidin appears to be superior to either supplementation alone on metabolic syndrome treatment , while the effects of flaxseed are stronger than hesperidin supplementation .

PURPOSE: The aim of the present study was to compare the clinical effect of flaxseed and hesperidin alone and with combination in patients with metabolic syndrome. Number of participants with treated metabolic syndrome was assessed as a primary end point.
METHODS: In this 12-week randomized controlled trial, ninety-eight patients with metabolic syndrome randomly assigned to receive either whole flaxseed powder (30 g/day), or hesperidin (1 g/day), or combination of 30 g flaxseed and 1 g hesperidin or no supplement while adhering a lifestyle modification program.
RESULTS: In comparison to control group, systolic blood pressure (- 5.68 vs. - 2.91 mmHg, P = 0.041) and serum concentrations of triglyceride (- 50.06 vs. 3.87 mg/dL, P = 0.033) in hesperidin group showed a significant reduction over 12 weeks of intervention. Comparison of the results of flaxseed group with the control group showed a significant improvement in serum concentrations of triglyceride (- 66 vs. 3.87 mg/dL, P = 0.028), insulin (- 4.27 vs. - 2.51 mU/L, P = 0.003) and accordingly insulin resistance (- 1.19 vs. - 0.76, P = 0.005) and sensitivity (0.03 vs. 0.01, P = 0.022) indices in flaxseed group. Combination of flaxseed and hesperidin improved three of five metabolic syndrome components including serum concentrations of triglyceride, glucose and systolic blood pressure as compared to placebo. Interestingly, co-administration of flaxseed and hesperidin with 77.3% reduction in the prevalence of defined metabolic syndrome was revealed to be most effective in controlling the metabolic syndrome, after which the group of flaxseed with 76% reduction and hesperidin group with 54.5% reduction were ranked second and third, respectively.
CONCLUSIONS: It can be concluded that co-administration of flaxseed and hesperidin appears to be superior to either supplementation alone on metabolic syndrome treatment, while the effects of flaxseed are stronger than hesperidin supplementation.


greenmedinfo--2020-07-01--Flaxseed may have a therapeutic effect on depression.

INTRODUCTION : Depression is a serious mental illness .
However , a significant proportion of patients with depression fail to @ @ @ @ @ .
This study was conducted to explore the antidepressant-like effect of flaxseed oil and flour @ @ @ @ @ depression-like behaviors induced by chronic unpredictable stress ( CUS ) .
METHODS : Rats were @ @ @ @ @ : normal control ( Sham-Sham ) , CUS plus saline ( S-SN ) , CUS @ @ @ @ @ , CUS plus flaxseeds oil ( S-FO ) , and CUS plus flaxseed flour ( @ @ @ @ @ tested using sucrose preference test and forced swimming test .
The serum BDNF concentration , @ @ @ @ @ protein expression were measured by enzyme-linked immunosorbent assay , real-time PCR , and Western blot @ @ @ @ @ The sucrose preference rate was significantly higher in S-FO and S-FF rats than in S-SN @ @ @ @ @ CONCLUSION : Flaxseed oil and flaxseed flour exert antidepressant-like effect in rats exposed to chronic @ @ @ @ @ a therapeutic effect on depression .

INTRODUCTION: Depression is a serious mental illness. However, a significant proportion of patients with depression fail to achieve remission with antidepressant therapies. This study was conducted to explore the antidepressant-like effect of flaxseed oil and flour in an animal model with depression-like behaviors induced by chronic unpredictable stress (CUS).
METHODS: Rats were randomly divided into five groups: normal control (Sham-Sham), CUS plus saline (S-SN), CUS plus escitalopram (S-Esc), CUS plus flaxseeds oil (S-FO), and CUS plus flaxseed flour (S-FF). Behaviors were tested using sucrose preference test and forced swimming test. The serum BDNF concentration, hippocampal BDNF mRNA, and protein expression were measured by enzyme-linked immunosorbent assay, real-time PCR, and Western blot, respectively.
RESULTS: The sucrose preference rate was significantly higher in S-FO and S-FF rats than in S-SN and S-Esc rats (p < .01), and lower in S-Esc rats than in Sham-Sham rats (p < .01). The immobility time was significantly shorter in S-FO and S-FF rats than in S-SN rats (p < .01), and shorter in S-Esc rats than in S-SN rats (p < .01). Plasma BDNF concentrations were significantly lower in S-FO, S-FF, and S-Esc rats than in Sham-Sham rats (p < .01); BDNF was lower in S-FO, S-FF, and S-SN rats than in S-Esc rats. The hippocampal BDNF protein expression was significantly higher in S-Esc rats than in S-SN rats (p < .05). The hippocampal BDNF mRNA expression was significantly higher in S-Esc rats than in S-SN rats (p < .01). The BDNF gene expression in plasma and the hippocampus negatively correlated with the immobility time (p < .05), but BDNF gene expression in the hippocampus positively correlated with the sucrose preference rate (p < .05).
CONCLUSION: Flaxseed oil and flaxseed flour exert antidepressant-like effect in rats exposed to chronic stress. Flaxseed may have a therapeutic effect on depression.


greenmedinfo--2020-07-01--Flaxseed supplementation may help to control cholesterol.

Being rich in polyunsaturated fatty acids , flaxseed ( L. ) is thought to be able to decrease lipid levels and dampen inflammation .
In this pilot study , we aimed to determine whether flaxseed supplementation could improve the profiles of lipids and inflammatory mediators in patients with severe hyperlipidemia resistant to conventional lipid-lowering pharmacotherapy and requiring lipoprotein apheresis .
To this end , six patients received , blindly-in addition to their normal lipoprotein apheresis regimen-a 10-week dietary supplementation with flaxseed ( 28 g/d ) administered in biscuits .
This was followed by a 10-week washed out-period and a 10-week @ @ @ @ @ @ @ Blood samples were collected at the end of each phase , before the lipoprotein apheresis session .
The primary endpoint was the lipid profile and the secondary endpoints were the concentrations of inflammatory mediators and tolerability .
Flaxseed supplementation was well-tolerated and resulted in a consistent and significant decrease in total cholesterol and low-density lipoprotein ( LDL ) levels .
The median ( and range ) percentage decrease was 11.5 % ( 0-18.8 ) and 7.3 % ( 4.4-26.6 ) , for cholesterol ( = 0.015 ) and LDL-C ( = 0.003 ) @ @ @ @ @ @ @ , there was no significant effect of flaxseed on lipoprotein ( a ) ( Lp ( a ) ) , C-reactive protein ( CRP ) , and interleukin 6 ( IL-6 ) concentrations .
These observations indicate that flaxseed can produce a cholesterol- and LDL-lowering effect in patients treated with lipoprotein apheresis .
Thus , flaxseed supplementation may help to control cholesterol in this patient population .
The flaxseed supplementation protocol applied may be of use for further adequately-powered studies to validate and extend our findings .

Being rich in polyunsaturated fatty acids, flaxseed (L.) is thought to be able to decrease lipid levels and dampen inflammation. In this pilot study, we aimed to determine whether flaxseed supplementation could improve the profiles of lipids and inflammatory mediators in patients with severe hyperlipidemia resistant to conventional lipid-lowering pharmacotherapy and requiring lipoprotein apheresis. To this end, six patients received, blindly-in addition to their normal lipoprotein apheresis regimen-a 10-week dietary supplementation with flaxseed (28 g/d) administered in biscuits. This was followed by a 10-week washed out-period and a 10-week supplementation phase with whole wheat placebo. Blood samples were collected at the end of each phase, before the lipoprotein apheresis session. The primary endpoint was the lipid profile and the secondary endpoints were the concentrations of inflammatory mediators and tolerability. Flaxseed supplementation was well-tolerated and resulted in a consistent and significant decrease in total cholesterol and low-density lipoprotein (LDL) levels. The median (and range) percentage decrease was 11.5% (0-18.8) and 7.3% (4.4-26.6), for cholesterol (= 0.015) and LDL-C (= 0.003), respectively. On the other hand, there was no significant effect of flaxseed on lipoprotein(a) (Lp(a)), C-reactive protein (CRP), and interleukin 6 (IL-6) concentrations. These observations indicate that flaxseed can produce a cholesterol- and LDL-lowering effect in patients treated with lipoprotein apheresis. Thus, flaxseed supplementation may help to control cholesterol in this patient population. The flaxseed supplementation protocol applied may be of use for further adequately-powered studies to validate and extend our findings.


greenmedinfo--2020-07-02--Anticancer activity of ursolic acid on human ovarian cancer cells.

PURPOSE : Ovarian cancer ( OC ) is perhaps the most difficult problem in gynaecologic oncology ; in particular the drug-resistant ovarian cancer remains a challenge for the clinicians .
Therefore there is a pressing need for novel and effective chemotherapeutic agents against OC .
The main objective of the current research work was to study the anticancer effects of a naturally occurring triterpene acid , ursolic acid , against SKOV-3 OC cells .
Its effects on reactive oxygen species ( ROS ) -mediated apoptosis were also studied along with cell cycle phase distribution and PI3K/AKT signalling pathway .
METHODS @ @ @ @ @ @ @ cell viability assay .
Apoptosis-related studies were examined by fluorescent microscopy using acridine orange ( AO ) /ethidium bromide ( EB ) and DAPI staining as well as flow cytometry using annexin V/propidium iodide ( PI ) assay .
Further , western blot assay was used to study effects of ursolic acid on the apoptosis-related protein expressions including Bax , Bcl-2 as well as PI3K/AKT signalling pathway .
Effects on cell cycle were examined by flow cytometry while effects on ROS production were evaluated by fluorescent microscopy .
RESULTS : Ursolic acid caused @ @ @ @ @ @ @ SKOV-3 ovarian carcinoma cells in a dose-dependent manner , exhibiting an IC50 of 35µM in cancer cells and IC50 of 75 µM in normal cell lines ( normal ovarian surface epithelial ( OSE ) .
Ursolic acid inhibited the viability of cancer cells via induction of apoptotic cell death which was associated with increase in Bax and decrease in Bcl-2 levels .
DAPI staining results also confirmed that ursolic acid induced apoptotic cell death .
Ursolic acid also induced dose-dependent G2/M phase cell cycle arrest along with causing significant upsurge in ROS production @ @ @ @ @ @ @ acid had the potential to inhibit I3K/AKT signalling pathway .
CONCLUSION : The results of this study clearly indicate that ursolic acid has the potential to be developed as a potent drug candidate against OC provided further in vivo and toxicological studies are carried out .

PURPOSE: Ovarian cancer (OC) is perhaps the most difficult problem in gynaecologic oncology; in particular the drug-resistant ovarian cancer remains a challenge for the clinicians. Therefore there is a pressing need for novel and effective chemotherapeutic agents against OC. The main objective of the current research work was to study the anticancer effects of a naturally occurring triterpene acid, ursolic acid, against SKOV-3 OC cells. Its effects on reactive oxygen species (ROS)-mediated apoptosis were also studied along with cell cycle phase distribution and PI3K/AKT signalling pathway.
METHODS: Cell proliferation was checked by CCK8 cell viability assay. Apoptosis-related studies were examined by fluorescent microscopy using acridine orange (AO)/ethidium bromide (EB) and DAPI staining as well as flow cytometry using annexin V/propidium iodide (PI) assay. Further, western blot assay was used to study effects of ursolic acid on the apoptosis-related protein expressions including Bax, Bcl-2 as well as PI3K/AKT signalling pathway. Effects on cell cycle were examined by flow cytometry while effects on ROS production were evaluated by fluorescent microscopy.
RESULTS: Ursolic acid caused significant reduction in the viability of the SKOV-3 ovarian carcinoma cells in a dose-dependent manner, exhibiting an IC50 of 35µM in cancer cells and IC50 of 75 µM in normal cell lines (normal ovarian surface epithelial (OSE). Ursolic acid inhibited the viability of cancer cells via induction of apoptotic cell death which was associated with increase in Bax and decrease in Bcl-2 levels. DAPI staining results also confirmed that ursolic acid induced apoptotic cell death. Ursolic acid also induced dose-dependent G2/M phase cell cycle arrest along with causing significant upsurge in ROS production. Western blot analysis revealed that ursolic acid had the potential to inhibit I3K/AKT signalling pathway.
CONCLUSION: The results of this study clearly indicate that ursolic acid has the potential to be developed as a potent drug candidate against OC provided further in vivo and toxicological studies are carried out.


greenmedinfo--2020-07-02--Ursolic acid potentiated oxaliplatin to induce apoptosis in colorectal cancer RKO cells.

Ursolic acid ( UA ) is found in multiple anticancer herbs and has shown anticancer effects in colorectal cancer ( @ @ @ @ @ present study aimed to observe the effects of a combination of UA and oxaliplatin ( @ @ @ @ @ used chemotherapeutic drug in CRC , on human CRC RKO cells .
The results showed @ @ @ @ @ inhibited the proliferation of RKO cells .
A combination of UA and Oxa induced apoptosis @ @ @ @ @ the activities of caspase-3 , caspase-8 , and caspase-9 .
Z-VAD-FMK , a caspase inhibitor @ @ @ @ @ Oxa-activated caspase-3 , caspase-8 , and caspase-9 and induced apoptosis .
In addition , UA @ @ @ @ @ of X-linked inhibitor of apoptosis ( XIAP ) and Survivin in RKO cells .
These @ @ @ @ @ of UA and Oxa elicited synergistically anticancer effects in RKO cells and provided new evidence @ @ @ @ @ and Oxa for CRC treatment .

Ursolic acid (UA) is found in multiple anticancer herbs and has shown anticancer effects in colorectal cancer (CRC) cells. The present study aimed to observe the effects of a combination of UA and oxaliplatin (Oxa), a frequently used chemotherapeutic drug in CRC, on human CRC RKO cells. The results showed that UA and Oxa synergistically inhibited the proliferation of RKO cells. A combination of UA and Oxa induced apoptosis in RKO cells and increased the activities of caspase-3, caspase-8, and caspase-9. Z-VAD-FMK, a caspase inhibitor, significantly antagonized UA- and Oxa-activated caspase-3, caspase-8, and caspase-9 and induced apoptosis. In addition, UA and Oxa downregulated the expression of X-linked inhibitor of apoptosis (XIAP) and Survivin in RKO cells. These observations suggested that a combination of UA and Oxa elicited synergistically anticancer effects in RKO cells and provided new evidence for potential application of UA and Oxa for CRC treatment.


greenmedinfo--2020-07-02--The anti-proliferative activity of ursolic acid in MDA-MB-231 human breast cancer cells.

The potential mechanisms of action of ursolic acid ( UA ) in regulating cell proliferation in MDA-MB-231 human breast cancer @ @ @ @ @ investigated .
UA significantly inhibited the proliferation of MDA-MB-231 cells at dose≥10 µM in a @ @ @ @ @ cytotoxicity was observed at concentrations below 29.87 ± 2.60 µM .
The expressions of Nrf2 @ @ @ @ @ and nucleus , and NQO1 were inhibited by UA treatment , while the Keap1 expression @ @ @ @ @ difference was observedin Nrf2 mRNA levels , indicating that UA reduced Nrf2 expression not through @ @ @ @ @ .
Additionally , EGF-induced p-Nrf2 and its downstream NQO1 and SOD1 enzymes were abolished by @ @ @ @ @ or p-EGFR had no effect on the expressions of Keap1 .
These results suggested that @ @ @ @ @ UA might be partially through down-regulating Nrf2 via Keap1/Nrf2 pathway and EGFR/Nrf2 pathway in MDA-MB-231 @ @

The potential mechanisms of action of ursolic acid (UA) in regulating cell proliferation in MDA-MB-231 human breast cancer cells through Nrf2 pathway were investigated. UA significantly inhibited the proliferation of MDA-MB-231 cells at dose≥10 µM in a dose-dependent manner, and no cytotoxicity was observed at concentrations below 29.87 ± 2.60 µM. The expressions of Nrf2 and p-Nrf2 in whole cell and nucleus, and NQO1 were inhibited by UA treatment, while the Keap1 expression was upregulated. No significant difference was observedin Nrf2 mRNA levels, indicating that UA reduced Nrf2 expression not through mRNA but a post-translational mechanism. Additionally, EGF-induced p-Nrf2 and its downstream NQO1 and SOD1 enzymes were abolished by UA. However, EGF or p-EGFR had no effect on the expressions of Keap1. These results suggested that the proliferative inhibitory effect of UA might be partially through down-regulating Nrf2 via Keap1/Nrf2 pathway and EGFR/Nrf2 pathway in MDA-MB-231 cells.


greenmedinfo--2020-07-02--Prunella vulgaris polysaccharides may interfere with hyperlipidaemia through anti-lipid peroxidation

Prunella vulgaris polysaccharides may interfere with hyperlipidaemia through anti-lipid peroxidation effects.

Prunella vulgaris polysaccharides ( PVPs ) have a variety of biological activities , but the mechanism and extent of their anti-hyperlipidaemic effect remain unclear .
In vitro , PVPs had a significant inhibitory effect on angiotensin ( Ang II ) -induced vascular smooth muscle cell ( VSMC ) proliferation .
A metabolomics approach based on gas chromatography-mass spectrometry ( GC-MS ) and chemometrics was established in this study to evaluate the anti-hyperlipidaemic activity of PVPs in a high-fat Sprague-Dawley rat model .
In vivo , PVPs could significantly reduce the weight gain and the increases in serum total cholesterol ( @ @ @ @ @ @ @ ) -C and non-high-density lipoprotein ( HDL ) -C levels observed in rats fed a high-fat diet ; they could also significantly increase serum GSH-Px activity , reduce the content of MDA and TNF-α and decrease abdominal fat volume in rats .
Furthermore , PVPs exerted a repairing effect on morphological and structural damage in liver tissue cells in hyperlipidaemic rats fed a high-fat diet .
PVPs improved lipid metabolism disorder in rats .
Alanine , threonine , succinic acid , proline , inositol and arachidonic acid levels in the serum were considered @ @ @ @ @ @ @ glucose , energy and lipid metabolism .
Therefore , PVPs may interfere with hyperlipidaemia through anti-lipid peroxidation effects , attenuation of inflammation and regulation of glucose , amino acid , energy and lipid metabolism .

Prunella vulgaris polysaccharides (PVPs) have a variety of biological activities, but the mechanism and extent of their anti-hyperlipidaemic effect remain unclear. In vitro, PVPs had a significant inhibitory effect on angiotensin (Ang II)-induced vascular smooth muscle cell (VSMC) proliferation. A metabolomics approach based on gas chromatography-mass spectrometry (GC-MS) and chemometrics was established in this study to evaluate the anti-hyperlipidaemic activity of PVPs in a high-fat Sprague-Dawley rat model. In vivo, PVPs could significantly reduce the weight gain and the increases in serum total cholesterol (TC), low-density lipoprotein (LDL)-C and non-high-density lipoprotein (HDL)-C levels observed in rats fed a high-fat diet; they could also significantly increase serum GSH-Px activity, reduce the content of MDA and TNF-α and decrease abdominal fat volume in rats. Furthermore, PVPs exerted a repairing effect on morphological and structural damage in liver tissue cells in hyperlipidaemic rats fed a high-fat diet. PVPs improved lipid metabolism disorder in rats. Alanine, threonine, succinic acid, proline, inositol and arachidonic acid levels in the serum were considered potential biomarkers involved in amino acid, glucose, energy and lipid metabolism. Therefore, PVPs may interfere with hyperlipidaemia through anti-lipid peroxidation effects, attenuation of inflammation and regulation of glucose, amino acid, energy and lipid metabolism.


greenmedinfo--2020-07-02--In vivo hepatoprotective potential of extracts obtained from floral spikes of Prunella vulgaris L

BACKGROUND : Prunella vulgaris , commonly known as self-heal , has been extensively used in the traditional system of medicines .
The plant has been found to contain a number of bioactive molecules including those having radical scavenging property which indicates its potential for the treatment of those diseases which are induced by free radical damage like drug-induced hepatotoxicity .
OBJECTIVE : The current study was undertaken to investigate the flavonoid and total phenolic content and evaluate the hepatoprotective potential of various extracts obtained from floral spikes of P. vulgaris .
MATERIAL AND METHODS : Flavonoid and otal phenolic contents @ @ @ @ @ @ @ Gallic acid as per the reported methods .
The extent of hepatotoxicity induced by paracetamol ( 500 mg/kg b.w , p.o daily for 14 days ) , hepatoprotective potential of extracts ( 200 mg/kg b.w/day , orally ) and standard drug silymarin ( 50 mg/kg b.w/day , orally ) were evaluated by analyzing various biochemical parameters like Serum Glutamic Oxaloacetic Transaminase , Serum Glutamic Pyruvic Transaminase , Alkaline Phosphatase , Total Proteins , Total and Direct Bilirubin and detailed histopathology of rat livers .
RESULTS : Methanolic extract showed higher quantity of flavonoids @ @ @ @ @ @ @ , hydroalcoholic and aqueous extracts .
Treatment of rats with extracts showed a highly significant reduction in the enzyme activities of Serum Glutamic Oxaloacetic Transaminase , Serum Glutamic Pyruvic Transaminase , Alkaline Phosphatase , and serum levels of Total , Direct Bilirubin ( P < 0.01 ) and highly significant elevation in Total Proteins ( P < 0.01 ) when compared with the toxic control group .
This was further confirmed by histopathological evaluation , where almost normal hepatic architecture or very less hepatic damage was observed in groups treated with extracts and @ @ @ @ @ @ @ Results from biochemical and histopathological evaluation indicated that among the extracts methanolic extract was most effective .
CONCLUSION : From the results , it can be concluded that the extracts obtained from floral spikes of P. vulgaris possess highly significant hepatoprotective activity which could be attributed to its radical scavenging potential and hepatic regeneration .
This is further authenticated by the presence of phenolic and flavonoids which are known to possess radical scavenging properties .

BACKGROUND: Prunella vulgaris, commonly known as self-heal, has been extensively used in the traditional system of medicines. The plant has been found to contain a number of bioactive molecules including those having radical scavenging property which indicates its potential for the treatment of those diseases which are induced by free radical damage like drug-induced hepatotoxicity.
OBJECTIVE: The current study was undertaken to investigate the flavonoid and total phenolic content and evaluate the hepatoprotective potential of various extracts obtained from floral spikes of P. vulgaris.
MATERIAL AND METHODS: Flavonoid and otal phenolic contents were obtained from the standard curves of Gallic acid as per the reported methods. The extent of hepatotoxicity induced by paracetamol (500 mg/kg b.w, p.o daily for 14 days), hepatoprotective potential of extracts (200 mg/kg b.w/day, orally) and standard drug silymarin (50 mg/kg b.w/day, orally) were evaluated by analyzing various biochemical parameters like Serum Glutamic Oxaloacetic Transaminase, Serum Glutamic Pyruvic Transaminase, Alkaline Phosphatase, Total Proteins, Total and Direct Bilirubin and detailed histopathology of rat livers.
RESULTS: Methanolic extract showed higher quantity of flavonoids and total phenolic content followed by ethanolic, hydroalcoholic and aqueous extracts. Treatment of rats with extracts showed a highly significant reduction in the enzyme activities of Serum Glutamic Oxaloacetic Transaminase, Serum Glutamic Pyruvic Transaminase, Alkaline Phosphatase, and serum levels of Total, Direct Bilirubin (P < 0.01) and highly significant elevation in Total Proteins (P < 0.01) when compared with the toxic control group. This was further confirmed by histopathological evaluation, where almost normal hepatic architecture or very less hepatic damage was observed in groups treated with extracts and silymarin compared to paracetamol treated group. Results from biochemical and histopathological evaluation indicated that among the extracts methanolic extract was most effective.
CONCLUSION: From the results, it can be concluded that the extracts obtained from floral spikes of P. vulgaris possess highly significant hepatoprotective activity which could be attributed to its radical scavenging potential and hepatic regeneration. This is further authenticated by the presence of phenolic and flavonoids which are known to possess radical scavenging properties.


greenmedinfo--2020-07-02--Prunella vulgaris protects glucocorticoids-induced osteogenesis inhibition in bone marrow mesenchyma

Prunella vulgaris protects glucocorticoids-induced osteogenesis inhibition in bone marrow mesenchymal stem cells.

OBJECTIVE : To elucidate the role of Prunella vulgaris L ( PVL ) in protecting glucocorticoids ( GC ) -induced osteogenesis inhibition , thereafter , protecting the deterioration of osteoporosis ( OP ) .
MATERIALS AND METHODS : Cell Counting Kit-8 ( CCK-8 ) assay was conducted to assess the influence of PVL treatment on MSCs viability .
Osteogenesis in MSCs was induced by Dexamethasone ( DEX ) stimulation .
Regulatory effects of PVL on osteogenesis-related gene expressions , ALP activity , and mineralization ability in DEX-induced MSCs were determined .
At last , protein levels of p-Smad1/5/9 and total-Smad1/5/9 @ @ @ @ @ @ @ by Western blot .
RESULTS : PVL treatment did not pose a time- or dose-dependent influence on MSCs viability .
DEX induction in MSCs downregulated ALP , RUNX2 , Bglap , and Osterix .
ALP activity and mineralization in DEX-induced MSCs were suppressed .
Downregulated osteogenesis-related genes decreased ALP activity and mineralization in MSCs undergoing DEX stimulation were partially reversed by PVL treatment .
Moreover , the downregulated p-Smad1/5/9 level in DEX-induced MSCs was elevated by PVL treatment , while total-Smad1/5/9 was not affected .
CONCLUSIONS : PVL alleviated GC-induced suppression in MSCs @ @ @ @ @ @ @ thereafter , protecting the deterioration of OP .

OBJECTIVE: To elucidate the role of Prunella vulgaris L (PVL) in protecting glucocorticoids (GC)-induced osteogenesis inhibition, thereafter, protecting the deterioration of osteoporosis (OP).
MATERIALS AND METHODS: Cell Counting Kit-8 (CCK-8) assay was conducted to assess the influence of PVL treatment on MSCs viability. Osteogenesis in MSCs was induced by Dexamethasone (DEX) stimulation. Regulatory effects of PVL on osteogenesis-related gene expressions, ALP activity, and mineralization ability in DEX-induced MSCs were determined. At last, protein levels of p-Smad1/5/9 and total-Smad1/5/9 influenced by DEX and PVL were measured by Western blot.
RESULTS: PVL treatment did not pose a time- or dose-dependent influence on MSCs viability. DEX induction in MSCs downregulated ALP, RUNX2, Bglap, and Osterix. ALP activity and mineralization in DEX-induced MSCs were suppressed. Downregulated osteogenesis-related genes decreased ALP activity and mineralization in MSCs undergoing DEX stimulation were partially reversed by PVL treatment. Moreover, the downregulated p-Smad1/5/9 level in DEX-induced MSCs was elevated by PVL treatment, while total-Smad1/5/9 was not affected.
CONCLUSIONS: PVL alleviated GC-induced suppression in MSCs osteogenesis by activating the Smad pathway, thereafter, protecting the deterioration of OP.


greenmedinfo--2020-07-02--Prunella vulgaris L. attenuates experimental autoimmune thyroiditis.

BACKGROUND : Prunella vulgaris L. ( P. vulgaris ) has traditionally been used to treat swelling and inflammation of the thyroid gland .
This study aimed to evaluate the effects of P. vulgaris on experimental autoimmune thyroiditis ( EAT ) and explore the roles of indoleamine 2,3-dioxygenase 1 ( IDO1 ) and regulatory T cells ( Tregs ) in these P. vulgaris-mediated effects .
METHODS : The main bioactive compounds in P. vulgaris were analysed by high-performance liquid chromatography .
An EAT model was established by immunization of Lewis rats with thyroglobulin via subcutaneous injection .
Thyroid volume was assessed @ @ @ @ @ @ @ the thyroid was evaluated by haematoxylin and eosin staining .
The serum levels of thyroglobulin antibody ( TgAb ) and cytokines were measured by indirect enzyme-linked immunosorbent assay .
The percentage of CD4CD25Foxp3Tregs was detected by flow cytometry .
The mRNA and protein levels of IDO1 were measured by qRT-PCR and Western blotting , respectively .
The levels of tryptophan ( Trp ) and kynurenine ( Kyn ) in serum and faecal samples were assessed with a fluorometric kit and spectrophotometry .
RESULTS : The main bioactive compound in P. vulgaris was rosmarinic @ @ @ @ @ @ @ volume in EAT rats were significantly decreased after administration of P. vulgaris ( P < 0.01 ) .
The inflammation score in EAT rats that were administered P. vulgaris was significantly lower than that in the EAT controls ( P < 0.01 ) .
In addition , P. vulgaris promoted the expansion of splenic Tregs and increased the production of IL-10 and TGF-β ( P < 0.01 ) in EAT rats .
Moreover , P. vulgaris induced IDO1 mRNA and protein expression in the spleen and intestine in P. vulgaris-treated EAT rats ( @ @ @ @ @ @ @ Trp levels were reduced and Kyn levels and the Kyn/Trp ratio were increased in the serum of P. vulgaris-treated EAT rats .
CONCLUSION : We were the first to demonstrate the role of IDO1-induced Treg expansion in P. vulgaris-mediated attenuation of EAT .
Our study provides insight into the immunopathogenesis of autoimmune thyroiditis and shows the potential therapeutic value of P. vulgaris .

BACKGROUND: Prunella vulgaris L. (P. vulgaris) has traditionally been used to treat swelling and inflammation of the thyroid gland. This study aimed to evaluate the effects of P. vulgaris on experimental autoimmune thyroiditis (EAT) and explore the roles of indoleamine 2,3-dioxygenase 1 (IDO1) and regulatory T cells (Tregs) in these P. vulgaris-mediated effects.
METHODS: The main bioactive compounds in P. vulgaris were analysed by high-performance liquid chromatography. An EAT model was established by immunization of Lewis rats with thyroglobulin via subcutaneous injection. Thyroid volume was assessed by ultrasound, and lymphatic infiltration in the thyroid was evaluated by haematoxylin and eosin staining. The serum levels of thyroglobulin antibody (TgAb) and cytokines were measured by indirect enzyme-linked immunosorbent assay. The percentage of CD4CD25Foxp3Tregs was detected by flow cytometry. The mRNA and protein levels of IDO1 were measured by qRT-PCR and Western blotting, respectively. The levels of tryptophan (Trp) and kynurenine (Kyn) in serum and faecal samples were assessed with a fluorometric kit and spectrophotometry.
RESULTS: The main bioactive compound in P. vulgaris was rosmarinic acid. The TgAb level and thyroid volume in EAT rats were significantly decreased after administration of P. vulgaris (P<0.01). The inflammation score in EAT rats that were administered P. vulgaris was significantly lower than that in the EAT controls (P<0.01). In addition, P. vulgaris promoted the expansion of splenic Tregs and increased the production of IL-10 and TGF-β (P<0.01) in EAT rats. Moreover, P. vulgaris induced IDO1 mRNA and protein expression in the spleen and intestine in P. vulgaris-treated EAT rats (P<0.01). Finally, Trp levels were reduced and Kyn levels and the Kyn/Trp ratio were increased in the serum of P. vulgaris-treated EAT rats.
CONCLUSION: We were the first to demonstrate the role of IDO1-induced Treg expansion in P. vulgaris-mediated attenuation of EAT. Our study provides insight into the immunopathogenesis of autoimmune thyroiditis and shows the potential therapeutic value of P. vulgaris.


greenmedinfo--2020-07-02--P. vulgaris L has marked anti- uterine myoma activity.

BACKGROUND : The flowers and dried fruit spikes of Prunella vulgaris L. ( P. vulgaris L. ) have been widely used in traditional Chinese medicine and food .
P. vulgaris L. is regarded as a good option for treating uterine myoma ( UM ) .
However , scientific evidence of anti-UM activity of the extract of P. vulgaris L. ( PVE ) is lacking .
The present study aimed to characterize the chemical composition of PVE and evaluate the pharmacodynamics and mechanism of PVE against UM .
METHODS : The chemical composition of PVE was analyzed by GC-MS. MTT was @ @ @ @ @ @ @ and toxicity .
Double fluorescence flow cytometry method were used to determine the apoptosis and cell cycle progression of UM cells under PVE treatment .
The anti-UM activity of PVE was investigated by using a specific-pathogen-free ( SPF ) rat model of UM .
TUNEL staining was used to detect the apoptosis of UM cells .
The concentrations of estrogen and progesterone in the serum of SPF rats were detected by ELISA .
The expression levels of PCNA , estrogen receptor alpha , estrogen receptor beta , progesterone receptor , survivin , caspase-3 @ @ @ @ @ @ @ of SPF rats was detected by immunohistochemistry ( IHC ) .
RESULTS : The extraction rate of PVE was 8.1 % .
The main components were squalene ( 28.3 % ) , linoleic acid ( 9.96 % ) , linolenic acid ( 9.95 % ) , stearic acid ( 6.26 % ) and oleic acid ( 5.51 % ) .
In vitro , PVE had significant anti-human UM cell activity , exhibited no drug toxicity , promoted the apoptosis of human UM cells , and inhibited the transition of UM cells from the @ @ @ @ @ @ @ in which DNA replication occurs .
In vivo , PVE had significant anti-UM activity .
PVE decreased the concentrations of estrogen and progesterone and downregulated the expression levels of the estrogen and progesterone receptors through the estrogen signaling pathway .
PVE also promoted the apoptosis of UM cells by downregulating the expression levels of the survivin and Bcl-2 proteins and upregulating the expression levels of caspase-3 and Bax through the mitochondria-mediated apoptotic pathway .
CONCLUSION : PVE has marked anti-UM activity .
PVE can be used as an ideal candidate drug to treat @ @

BACKGROUND: The flowers and dried fruit spikes of Prunella vulgaris L. (P. vulgaris L.) have been widely used in traditional Chinese medicine and food. P. vulgaris L. is regarded as a good option for treating uterine myoma (UM). However, scientific evidence of anti-UM activity of the extract of P. vulgaris L. (PVE) is lacking. The present study aimed to characterize the chemical composition of PVE and evaluate the pharmacodynamics and mechanism of PVE against UM.
METHODS: The chemical composition of PVE was analyzed by GC-MS. MTT was used to screen and evaluate cell proliferation and toxicity. Double fluorescence flow cytometry method were used to determine the apoptosis and cell cycle progression of UM cells under PVE treatment. The anti-UM activity of PVE was investigated by using a specific-pathogen-free (SPF) rat model of UM. TUNEL staining was used to detect the apoptosis of UM cells. The concentrations of estrogen and progesterone in the serum of SPF rats were detected by ELISA. The expression levels of PCNA, estrogen receptor alpha, estrogen receptor beta, progesterone receptor, survivin, caspase-3, Bax and Bcl-2 in the uterus of SPF rats was detected by immunohistochemistry (IHC).
RESULTS: The extraction rate of PVE was 8.1%. The main components were squalene (28.3%), linoleic acid (9.96%), linolenic acid (9.95%), stearic acid (6.26%) and oleic acid (5.51%). In vitro, PVE had significant anti-human UM cell activity, exhibited no drug toxicity, promoted the apoptosis of human UM cells, and inhibited the transition of UM cells from the G0/G1 stage into the G2 stage, in which DNA replication occurs. In vivo, PVE had significant anti-UM activity. PVE decreased the concentrations of estrogen and progesterone and downregulated the expression levels of the estrogen and progesterone receptors through the estrogen signaling pathway. PVE also promoted the apoptosis of UM cells by downregulating the expression levels of the survivin and Bcl-2 proteins and upregulating the expression levels of caspase-3 and Bax through the mitochondria-mediated apoptotic pathway.
CONCLUSION: PVE has marked anti-UM activity. PVE can be used as an ideal candidate drug to treat UM.


greenmedinfo--2020-07-02--Beneficial effects of flaxseed polysaccharides on metabolic syndrome.

Flaxseed ( Linum usitatissimum L. ) is known as healthy food for its anti-obesity and lipid modulating properties .
However @ @ @ @ @ polysaccharide ( FSP ) on metabolic syndrome ( MetS ) and gut microbiota are still @ @ @ @ @ we investigated the effects of FSP on lipid metabolism and gut microbiota in high-fat-diet-fed mice @ @ @ @ @ serum fasting glucose , total triglyceride and total cholesterol levels .
FSP consumption adipose accumulation @ @ @ @ @ different taxonomic levels by increasing the proportions of beneficial Akkermansia and Bifidobacterium and decreasing the @ @ @ @ @ and Odoribacteraceae .
These changes were highly correlated with the regulation of expression levels of @ @ @ @ @ the liver .
The restoration of total SCFAs , especially propionate and butyrate might be @ @ @ @ @ HFD induced metabolic disorders .
These findings suggest that FSP may use as a prebiotic @ @ @ @ @ the gut microbiota .

Flaxseed (Linum usitatissimum L.) is known as healthy food for its anti-obesity and lipid modulating properties. However, the effects of flaxseed polysaccharide (FSP) on metabolic syndrome (MetS) and gut microbiota are still poorly understood. Here, we investigated the effects of FSP on lipid metabolism and gut microbiota in high-fat-diet-fed mice. FSP effectively reduced the serum fasting glucose, total triglyceride and total cholesterol levels. FSP consumption adipose accumulation impacted the gut microbiome at different taxonomic levels by increasing the proportions of beneficial Akkermansia and Bifidobacterium and decreasing the disease or obesity associated Oscillospira and Odoribacteraceae. These changes were highly correlated with the regulation of expression levels of lipid metabolism involved genes in the liver. The restoration of total SCFAs, especially propionate and butyrate might be an important strategy for mitigating HFD induced metabolic disorders. These findings suggest that FSP may use as a prebiotic for preventing MetS by modulating the gut microbiota.


greenmedinfo--2020-07-02--Orbitides isolated from flaxseed induce apoptosis against SGC-7901 adenocarcinoma cells.

Unique plant-derived cyclic peptides family exhibiting various key biological activities has great possibility for anticancer therapy .
In this study @ @ @ @ @ of orbitides isolated from flax ( L. ) on the growth of SGC-7901 cancer cells @ @ @ @ @ Results showed that flaxseed orbitides killed off cancer cells by inducing apoptosis in a dose-dependent @ @ @ @ @ by the appearance of nuclear shrinkage and DNA fragmentation , and the inhibitory effect was @ @ @ @ @ orbitide [ 1-9-NαC ] -linusorb B2 or [ 1-9-NαC ] -linusorb B3 .
Besides , @ @ @ @ @ cytochrome C ( Cyt C ) was released from mitochondria to cytosol , associated with @ @ @ @ @ and 3 , and the cleavage of PARP .
Taken together , these results indicated @ @ @ @ @ the mitochondrial pathway , releasing Cyt C , increasing Bax/Bcl-2 ratio and elevating the expression @ @ @ @ @ 3 in SGC-7901 cells .

Unique plant-derived cyclic peptides family exhibiting various key biological activities has great possibility for anticancer therapy. In this study, we investigated the effects of orbitides isolated from flax (L.) on the growth of SGC-7901 cancer cells and the potential mechanism. Results showed that flaxseed orbitides killed off cancer cells by inducing apoptosis in a dose-dependent manner, which was confirmed by the appearance of nuclear shrinkage and DNA fragmentation, and the inhibitory effect was stronger than that of pure orbitide [1-9-NαC]-linusorb B2 or [1-9-NαC]-linusorb B3. Besides, the mitochondrial apoptosis pathway-related protein cytochrome C (Cyt C) was released from mitochondria to cytosol, associated with the activation of caspases 9 and 3, and the cleavage of PARP. Taken together, these results indicated that flaxseedorbitides induced apoptosis via the mitochondrial pathway, releasing Cyt C, increasing Bax/Bcl-2 ratio and elevating the expression of cleaved caspase 9 and 3 in SGC-7901 cells.


greenmedinfo--2020-07-02--Hesperidin may be an effective medicine for post-traumatic stress disorder.

OBJECTIVE : Post-traumatic stress disorder ( PTSD ) is a psychiatric disorder characterized by depression and anxiety , that arises due to an imbalance of neurotransmitters in response to excessive stress .
Hesperidin ( HSD ) is a naturally occurring flavonoid shown to exert a variety of biological activities , including antioxidant , anti-inflammatory , and neuroprotective effects .
METHODS : This study was used the open field test ( OFT ) and forced swimming test ( FST ) to examine the effects of HSD on the depression-like response of rats after exposure to a single prolonged stress ( SPS @ @ @ @ @ @ @ serotonergic activation system .
Male rats were given HSD ( 20 , 50 , and 100 mg/kg , intraperitoneal injection , n=6-7 per group ) once daily for 14 days after exposure to SPS .
The influence of administration of HSD on SPS-induced behavioral responses and concentrations of serotonin ( 5-HT ) , 5-hydroxyindoleacetic acid ( 5-HIAA ) , and monoamine oxidase-A ( MAO-A ) in the rat brain were also investigated using enzyme-linked immunoassays ( ELISAs ) .
RESULTS : Daily HSD administration signifificantly improved depression-like behaviors in the FST ( P0.05 @ @ @ @ @ @ @ crossed in the central zone of the OFT ( P0.01 ) , and reduced freezing behavior both in contextual and cued fear conditioning .
HSD treatment also attenuated the reduction in SPS-induced 5-HT concentrations in the hippocampus and amygdala .
This increase in 5-HT concentrations during HSD treatment was partially attributed to a decrease in the 5-HIAA/5-HT ratio in the hippocampus of rats with PTSD .
Furthermore , HSD treatment inhibited activity of MAO-A and decreases of tryptophan hydroxylase-1 expression in the hippocampus .
CONCLUSION : HSD was shown to exert antidepressant effects @ @ @ @ @ @ @ that this natural flflavonoid may be an effective medicine for PTSD .

OBJECTIVE: Post-traumatic stress disorder (PTSD) is a psychiatric disorder characterized by depression and anxiety, that arises due to an imbalance of neurotransmitters in response to excessive stress. Hesperidin (HSD) is a naturally occurring flavonoid shown to exert a variety of biological activities, including antioxidant, anti-inflammatory, and neuroprotective effects.
METHODS: This study was used the open field test (OFT) and forced swimming test (FST) to examine the effects of HSD on the depression-like response of rats after exposure to a single prolonged stress (SPS) leading to the dysregulation of the serotonergic activation system. Male rats were given HSD (20, 50, and 100 mg/kg, intraperitoneal injection, n=6-7 per group) once daily for 14 days after exposure to SPS. The influence of administration of HSD on SPS-induced behavioral responses and concentrations of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and monoamine oxidase-A (MAO-A) in the rat brain were also investigated using enzyme-linked immunoassays (ELISAs).
RESULTS: Daily HSD administration signifificantly improved depression-like behaviors in the FST (P0.05), increased the number of lines crossed in the central zone of the OFT (P0.01), and reduced freezing behavior both in contextual and cued fear conditioning. HSD treatment also attenuated the reduction in SPS-induced 5-HT concentrations in the hippocampus and amygdala. This increase in 5-HT concentrations during HSD treatment was partially attributed to a decrease in the 5-HIAA/5-HT ratio in the hippocampus of rats with PTSD. Furthermore, HSD treatment inhibited activity of MAO-A and decreases of tryptophan hydroxylase-1 expression in the hippocampus.
CONCLUSION: HSD was shown to exert antidepressant effects in rats exposed to SPS, suggesting that this natural flflavonoid may be an effective medicine for PTSD.


greenmedinfo--2020-07-01--Hesperidin ameliorates anxiety-depressive-like behaviour.

The mechanisms underlying the neuroprotective effects of hesperidin in a murine model of PD are not fully elucidated .
The @ @ @ @ @ to investigate the ability of hesperidin in modulating proinflammatory cytokines , neurotrophic factors , and @ @ @ @ @ 6-OHDA ) -induced nigral dopaminergic neuronal loss .
Adult male C57BL/6 mice were randomly assigned @ @ @ @ @ I ) sham/vehicle , ( II ) sham/hesperidin , ( III ) 6-OHDA/vehicle , and @ @ @ @ @ Mice received a unilateral intrastriatal injection of 6-OHDA and treated with hesperidin ( 50 mg/kg @ @ @ @ @ 28 days .
After hesperidin treatment , mice were submitted to behavioral tests and had @ @ @ @ @ assays .
Our results demonstrated that oral treatment with hesperidin ameliorated the anxiety-related and depressive-like @ @ @ @ @ p

The mechanisms underlying the neuroprotective effects of hesperidin in a murine model of PD are not fully elucidated. The current study was carried out to investigate the ability of hesperidin in modulating proinflammatory cytokines, neurotrophic factors, and neuronal recovery in 6-hydroxydopamine (6-OHDA)-induced nigral dopaminergic neuronal loss. Adult male C57BL/6 mice were randomly assigned into four groups: (I) sham/vehicle, (II) sham/hesperidin, (III) 6-OHDA/vehicle, and (IV) 6-OHDA/hesperidin. Mice received a unilateral intrastriatal injection of 6-OHDA and treated with hesperidin (50 mg/kg; per oral) for 28 days. After hesperidin treatment, mice were submitted to behavioral tests and had the striatum removed for neurochemical assays. Our results demonstrated that oral treatment with hesperidin ameliorated the anxiety-related and depressive-like behaviors in 6-OHDA-lesioned mice (p < 0.05). It also attenuated the striatal levels of proinflammatory cytokines tumor necrosis factor-α, interferon-gamma, interleukin-1β, interleukin-2, and interleukin-6 and increased the levels of neurotrophic factors, including neurotrophin-3, brain-derived neurotrophic factor, and nerve growthfactor in the striatum of 6-OHDA mice (p < 0.05). Hesperidin treatment was also capable to increase striatal levels of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid and protects against the impairment of dopaminergic neurons in the substantia nigra pars compacta (SNpc) (p < 0.05). In conclusion, this study indicated that hesperidin exerts anxiolytic-like and antidepressant-like effect against 6-OHDA-induced neurotoxicity through the modulation of cytokine production, neurotrophic factors levels, and dopaminergic innervation in the striatum.


greenmedinfo--2020-07-01--Hesperidin was effective in reducing signs of metabolic syndrome and alterations of left ventricular

Hesperidin was effective in reducing signs of metabolic syndrome and alterations of left ventricular hypertrophy and function.

BACKGROUND : Hesperidin has been reported to have biological activities such as antihypertensive , hypoglycemic , and antioxidant effects .
@ @ @ @ @ could improve signs of the metabolic syndrome and cardiac function in a high-fat diet ( @ @ @ @ @ ( MS ) in rats .
METHODS : Male Sprague-Dawley rats were fed HFD and @ @ @ @ @ weeks and treated with hesperidin ( 15 or 30 mg/kg , based on signs of @ @ @ @ @ ) or metformin , a positive control agent , ( 100 mg/kg ) for the @ @ @ @ @ function , blood pressure , fasting blood glucose , oral glucose tolerance , serum insulin @ @ @ @ @ .
Histomorphometrics of left ventricles , epidydimal fat pads and liver were evaluated .
Expressions @ @ @ @ @ ( p-IRS1 ) , p-Akt and GLUT4 in cardiac tissue were determined .
CONCLUSION : @ @ @ @ @ signs of MS and alterations of LV hypertrophy and function .
These beneficial effects on @ @ @ @ @ the restoration of the cardiac insulin signaling pathway in MS rats .

BACKGROUND: Hesperidin has been reported to have biological activities such as antihypertensive, hypoglycemic, and antioxidant effects. This study investigated whether hesperidin could improve signs of the metabolic syndrome and cardiac function in a high-fat diet (HFD) induced metabolic syndrome (MS) in rats.
METHODS: Male Sprague-Dawley rats were fed HFD and 15% fructose for 16 weeks and treated with hesperidin (15 or 30 mg/kg, based on signs of MS from a preliminary study) or metformin, a positive control agent, (100 mg/kg) for the final four weeks. Cardiac function, blood pressure, fasting blood glucose, oral glucose tolerance, serum insulin, and lipid profiles weremeasured. Histomorphometrics of left ventricles, epidydimal fat pads and liver were evaluated. Expressions of phosphorylate insulin receptor substrate1(p-IRS1), p-Akt and GLUT4 in cardiac tissue were determined.
RESULTS: Hesperidin and metformin attenuated MS in HFD rats (p < 0.05). The accumulation of visceral fat pads and fatty liver associated with increases in liver lipid contents and liver enzymes were found in MS rats that were alleviated in hesperidin or metformin-treated groups (p < 0.05). Hesperidin and metformin improved cardiac dysfunction and hypertrophy observed in MS rats (p < 0.05). Restoration of the insulin signaling pathway, IRS/Akt/GLUT4 protein expression, was demonstrated in hesperidin and metformin-treated groups (p < 0.05). Hesperidin (30 mg/kg) was more effective than the lower dose.
CONCLUSION: Hesperidin was effective in reducing signs of MS and alterations of LV hypertrophy and function. These beneficial effects on the heart were associated with the restoration of the cardiac insulin signaling pathway in MS rats.


greenmedinfo--2020-07-01--Hesperidin protects against renal injury induced by ischemia/reperfusion.

Renal injury is reported to have a high mortality rate .
Additionally , there are several limitations to current conventional treatments that are used to manage it .
This study evaluated the protective effect of hesperidin against ischemia/reperfusion ( I/R ) -induced kidney injury in rats .
Renal injury was induced by generating I/R in kidney tissues .
Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days .
The effect of hesperidin on renal function , serum mediators of inflammation , and levels of @ @ @ @ @ @ @ in rat kidney tissues after I/R-induced kidney injury .
Moreover , protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR .
Hematoxylin and eosin ( H & E ) staining was done for histopathological observation of kidney tissues .
The data suggest that the levels of blood urea nitrogen ( BUN ) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group .
Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats .
@ @ @ @ @ @ @ NF-κB p65 , Toll-like receptor 4 ( TLR-4 ) protein , TLR-4 mRNA , and inducible nitric oxide synthase ( iNOS ) was significantly reduced in the renal tissues of hesperidin-treated rats .
Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury inI/R kidney-injured rats .
In conclusion , our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling .

Renal injury is reported to have a high mortality rate. Additionally, there are several limitations to current conventional treatments that are used to manage it. This study evaluated the protective effect of hesperidin against ischemia/reperfusion (I/R)-induced kidney injury in rats. Renal injury was induced by generating I/R in kidney tissues. Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days. The effect of hesperidin on renal function, serum mediators of inflammation, and levels of oxidative stress in renal tissues were observed in rat kidney tissues after I/R-induced kidney injury. Moreover, protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR. Hematoxylin and eosin (H&E) staining was done for histopathological observation of kidney tissues. The data suggest that the levels of blood urea nitrogen (BUN) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group. Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats. The expression of p-IκBα, caspase-3, NF-κB p65, Toll-like receptor 4 (TLR-4) protein, TLR-4 mRNA, and inducible nitric oxide synthase (iNOS) was significantly reduced in the renal tissues of hesperidin-treated rats. Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury inI/R kidney-injured rats. In conclusion, our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling.