greenmedinfo--2020-08-28--Okra consumption can elicit improvements in lipid profile, as well as glycemic markers, among T2D pa

Okra consumption can elicit improvements in lipid profile, as well as glycemic markers, among T2D patients.

The aim of the present study was to investigate the effect of okra consumption on serum levels of lipid profiles and glycemic indices in Type 2 diabetic ( T2D ) patients .
The present study was a randomized , double-blinded clinical trial , carried out in Kerman , Iran .
Sixty T2D patients were randomized into intervention and control groups and received 10 g okra powder blended in 150 g conventional yogurt or conventional yogurt alone , along with dinner and lunch , for 8 weeks .
Glycemic markers and lipid profile were assessed , as well as anthropometric measures @ @ @ @ @ @ @ study .
The findings showed that 8 weeks okra consumption resulted in a significant decrease in fasting plasma glucose ( -15.61 ± 19.44 vs. -3.40 ± 24.78 ; p = .02 ) , homeostatic model of assessment for insulin resistance ( -1.17 ± 1.61 vs. -0.14 ± 1.64 ; p = .01 ) , quantitative insulin sensitivity check index ( 0.01 ± 0.007 vs. 0.00 ± 0.01 ; p = .004 ) , triacylglycerol ( -22.30 ± 32.46 vs. -3.86 ± 30.57 ; p = .001 ) , total cholesterol ( -10.23 ± @ @ @ @ @ @ @ = .004 ) , low-density lipoprotein cholesterol ( LDL-C ; -8.15 ± 10.01 vs. -2.31 ± 9.37 ; p = .02 ) , and LDL-C/high-density lipoprotein cholesterol ( HDL-C ) ratio ( -0.28 ± 0.37 vs. -0.08 ± 0.24 ; p = .01 ) .
No significant difference was observed between groups in HDL-C , glycated hemoglobin , fasting insulin levels , and anthropometric measures .
The present study suggests that okra consumption can elicit improvements in lipid profile , as well asglycemic markers , among T2D patients .

The aim of the present study was to investigate the effect of okra consumption on serum levels of lipid profiles and glycemic indices in Type 2 diabetic (T2D) patients. The present study was a randomized, double-blinded clinical trial, carried out in Kerman, Iran. Sixty T2D patients were randomized into intervention and control groups and received 10 g okra powder blended in 150 g conventional yogurt or conventional yogurt alone, along with dinner and lunch, for 8 weeks. Glycemic markers and lipid profile were assessed, as well as anthropometric measures, at the beginning and end of study. The findings showed that 8 weeks okra consumption resulted in a significant decrease in fasting plasma glucose (-15.61 ± 19.44 vs. -3.40 ± 24.78; p = .02), homeostatic model of assessment for insulin resistance (-1.17 ± 1.61 vs. -0.14 ± 1.64; p = .01), quantitative insulin sensitivity check index (0.01 ± 0.007 vs. 0.00 ± 0.01; p = .004), triacylglycerol (-22.30 ± 32.46 vs. -3.86 ± 30.57; p = .001), total cholesterol (-10.23 ± 10.36 vs. -2.03 ± 13.94; p = .004), low-density lipoprotein cholesterol (LDL-C; -8.15 ± 10.01 vs. -2.31 ± 9.37; p = .02), and LDL-C/high-density lipoprotein cholesterol (HDL-C)ratio (-0.28 ± 0.37 vs. -0.08 ± 0.24; p = .01). No significant difference was observed between groups in HDL-C, glycated hemoglobin, fasting insulin levels, and anthropometric measures. The present study suggests that okra consumption can elicit improvements in lipid profile, as well asglycemic markers, among T2D patients.


greenmedinfo--2020-08-28--Abelmoschus esculentus peel powder improves high-fat-diet-induced cognitive impairment.

Okra peel exhibits numerous therapeutic effects .
This study explores the potential ameliorative effects of okra peel powder on high-fat-diet ( HFD ) -induced hypercholesterolemia and cognitive deficits .
Thirty-six C57BL/6J male mice were randomly divided into six groups ( = 6 per group ) : ( i ) control , mice fed with a normal diet ; ( ii ) HFD , mice fed with HFD ; ( iii ) HFD-SIM , mice fed with HFD and given simvastatin ( 20 mg/kg/day ) ; ( iv ) HFD-OP1 ; ( v ) HFD-OP2 ; ( vi ) HFD-OP3 , @ @ @ @ @ @ @ ( 200 , 400 , or 800 mg/kg/day , respectively ) .
Following 10 weeks of treatments , the mice were subjected to the Morris water maze ( MWM ) .
Parameters such as weekly average body weight , food intake , and blood lipid profiles were also recorded .
The HFD group showed a profound increase in total cholesterol and low-density lipoprotein concentration compared to the control group .
All okra-treated and HFD-SIM groups performed better than the HFD group during acquisition trials , whereas only the HFD-OP1 produced a significantly higher @ @ @ @ @ @ @ during the probe trial .
In sum , all three okra doses improved the learning ability of the mice .
However , only the lowest dose of okra significantly improved the spatial reference memory retention .

Okra peel exhibits numerous therapeutic effects. This study explores the potential ameliorative effects of okra peel powder on high-fat-diet (HFD)-induced hypercholesterolemia and cognitive deficits. Thirty-six C57BL/6J male mice were randomly divided into six groups (= 6 per group): (i) control, mice fed with a normal diet; (ii) HFD, mice fed with HFD; (iii) HFD-SIM, mice fed with HFD and given simvastatin (20 mg/kg/day); (iv) HFD-OP1; (v) HFD-OP2; (vi) HFD-OP3, mice fed with HFD and okra peel (200, 400, or 800 mg/kg/day, respectively). Following 10 weeks of treatments, the mice were subjected to the Morris water maze (MWM). Parameters such as weekly average body weight, food intake, and blood lipid profiles were also recorded. The HFD group showed a profound increase in total cholesterol and low-density lipoprotein concentration compared to the control group. All okra-treated and HFD-SIM groups performed better than the HFD group during acquisition trials, whereas only the HFD-OP1 produced a significantly higher number of entries into the platform zone during the probe trial. In sum, all three okra doses improved the learning ability of the mice. However, only the lowest dose of okra significantly improved the spatial reference memory retention.


greenmedinfo--2020-08-28--Sesamol protects MIN6 pancreatic beta cells against simvastatin-induced toxicity by restoring mitoch

Sesamol protects MIN6 pancreatic beta cells against simvastatin-induced toxicity by restoring mitochondrial membrane potentials.

Statins , the drugs for the treatment of dyslipidemia , have been suggested to impact insulin sensitivity , resulting in pancreaticβ-cell dysfunction , and consequently , lead to new onset of diabetes .
Taking this as a clue , the present study was designed to evaluate the protective effect of sesamol ( a known antioxidant , antidiabetic and antidyslipidemic agent ) against the diabetogenic potential of simvastatin .
The toxic effectsof simvastatin and sesamol on MIN6 insulinoma ( Mouse pancreatic β cells ) cells were evaluated separately by MTT assay .
The protective effect of sesamol was evaluated at the @ @ @ @ @ @ @ 7.8 to 62.5 micromolar ( µM ) .
Further , the reversal of the impact of simvastatin on cell cycle and mitochondrial membrane potential by sesamol pretreatment was studied .
The ICfor simvastatin and sesamol were found to be 70.05 ± 2.34 μM and 2134 ± 8.41 μM , respectively , after 48 h and 72 h of incubation .
Sesamol pretreatment protected the MIN6 cells from simvastatin toxicity ( 70 µM ) in a dose-dependent manner from 7.8 to 31.25 µM .
Simvastatin induced cell cycle arrest in G/Gphase .
However , @ @ @ @ @ @ @ 24 h , a reversal in the cell cycle arrest was observed in simvastatin-treated cells ( G/G ) .
Pretreatment with sesamol also reduced the mitochondrial membrane potential loss compared to simvastatin treatment alone .
These in vitro findings indicate that sesamol has a protective effect against simvastatin-induced toxicity on the pancreatic beta cells .

Statins, the drugs for the treatment of dyslipidemia, have been suggested to impact insulin sensitivity, resulting in pancreaticβ-cell dysfunction, and consequently, lead to new onset of diabetes. Taking this as a clue, the present study was designed to evaluate the protective effect of sesamol (a known antioxidant, antidiabetic and antidyslipidemic agent) against the diabetogenic potential of simvastatin. The toxic effectsof simvastatin and sesamol on MIN6 insulinoma (Mouse pancreatic β cells) cells were evaluated separately by MTT assay. The protective effect of sesamol was evaluated at the ICvalue of simvastatin at doses ranging from 7.8 to 62.5 micromolar (µM). Further, the reversal of the impact of simvastatin on cell cycle and mitochondrial membrane potential by sesamol pretreatment was studied. The ICfor simvastatin and sesamol were found to be 70.05 ± 2.34 μM and 2134 ± 8.41 μM, respectively, after 48 h and 72 h of incubation. Sesamol pretreatment protected the MIN6 cells from simvastatin toxicity (70 µM) in a dose-dependent manner from 7.8 to 31.25 µM. Simvastatin induced cell cycle arrest in G/Gphase. However, when cells were preincubated with sesamol for 24 h, a reversal in the cell cycle arrest was observed in simvastatin-treated cells (G/G). Pretreatment with sesamol also reduced the mitochondrial membrane potential loss compared to simvastatin treatment alone. These in vitro findings indicate that sesamol has a protective effect against simvastatin-induced toxicity on the pancreatic beta cells.


greenmedinfo--2020-08-28--Sesamol alleviates airway hyperresponsiveness and oxidative stress in asthmatic mice.

Sesamol , isolated from sesame seeds , was previously shown to have antioxidative , anti-inflammatory , and anti-tumor effects .
Sesamol also inhibited lipopolysaccharide ( LPS ) -induced pulmonary inflammatory response in rats .
However , it remains unclear how sesamol regulates airway inflammation and oxidative stress in asthmatic mice .
This study aimed to investigate the efficacy of sesamol on oxidative stress and airway inflammation in asthmatic mice and tracheal epithelial cells .
BALB/c mice were sensitized with ovalbumin , and received oral sesamol on days 14 to 27 .
Furthermore , BEAS-2B human bronchial epithelial cells were treated @ @ @ @ @ @ @ and oxidative responses in vitro .
Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung , airway hyperresponsiveness , and T helper 2 cell-associated ( Th2 ) cytokine expressions in bronchoalveolar lavage fluid and the lungs .
Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice .
We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells .
Moreover , sesamol alleviated reactive oxygen species formation , and suppressed intercellular cell adhesion molecule-1 ( ICAM-1 @ @ @ @ @ @ @ adherence .
We demonstrated that sesamol showed potential as a therapeutic agent for improving asthma .

Sesamol, isolated from sesame seeds, was previously shown to have antioxidative, anti-inflammatory, and anti-tumor effects. Sesamol also inhibited lipopolysaccharide (LPS)-induced pulmonary inflammatory response in rats. However, it remains unclear how sesamol regulates airway inflammation and oxidative stress in asthmatic mice. This study aimed to investigate the efficacy of sesamol on oxidative stress and airway inflammation in asthmatic mice and tracheal epithelial cells. BALB/c mice were sensitized with ovalbumin, and received oral sesamol on days 14 to 27. Furthermore, BEAS-2B human bronchial epithelial cells were treated with sesamol to investigate inflammatory cytokine levels and oxidative responses in vitro. Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung, airway hyperresponsiveness, and T helper 2 cell-associated (Th2) cytokine expressions in bronchoalveolar lavage fluid and the lungs. Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice. We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells. Moreover, sesamol alleviated reactive oxygen species formation, and suppressed intercellular cell adhesion molecule-1 (ICAM-1) expression, which reduced monocyte cell adherence. We demonstrated that sesamol showed potential as a therapeutic agent for improving asthma.


greenmedinfo--2020-08-28--These findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expendit

These findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expenditure.

Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism .
However , its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated .
In this study , we show that sesamol increased the uncoupling protein 1 ( Ucp1 ) expression in adipocytes .
The administration of sesamol in high-fat diet ( HFD ) -fed mice prevented weight gain and improved metabolic derangements .
The three-week sesamol treatment of HFD-fed mice , when the body weights were not different between the sesamol and control groups , increased energy expenditure , @ @ @ @ @ @ @ a primary contributing factor for sesamol 's anti-obese effects .
Consistently , sesamol induced the expression of energy-dissipating thermogenic genes , including , in white adipose tissues .
The microarray analysis showed that sesamol dramatically increased the Nrf2 target genes such as Hmox1 and Atf3 in adipocytes .
Moreover , 76 % ( 60/79 genes ) of the sesamol-induced genes were also regulated by tert-butylhydroquinone ( tBHQ ) , a known Nrf2 activator .
We further verified that sesamol directly activated the Nrf2-mediated transcription .
In addition , the Hmox1 and Ucp1 induction @ @ @ @ @ @ @ , indicating the necessity of Nrf2 in the sesamol-mediated Ucp1 induction .
Together , these findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expenditure , further highlighting the use of the Nrf2 activation in stimulating thermogenic adipocytes and in increasing energy expenditure in obesity and its related metabolic diseases .

Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism. However, its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated. In this study, we show that sesamol increased the uncoupling protein 1 (Ucp1) expression in adipocytes. The administration of sesamol in high-fat diet (HFD)-fed mice prevented weight gain and improved metabolic derangements. The three-week sesamol treatment of HFD-fed mice, when the body weights were not different between the sesamol and control groups, increased energy expenditure, suggesting that an induced energy expenditure is a primary contributing factor for sesamol's anti-obese effects. Consistently, sesamol induced the expression of energy-dissipating thermogenic genes, including, in white adipose tissues. The microarray analysis showed that sesamol dramatically increased the Nrf2 target genes such as Hmox1 and Atf3 in adipocytes. Moreover, 76% (60/79 genes) of the sesamol-induced genes were also regulated by tert-butylhydroquinone (tBHQ), a known Nrf2 activator. We further verified that sesamol directly activated the Nrf2-mediated transcription. In addition, the Hmox1 and Ucp1 induction by sesamol was compromised in Nrf2-deleted cells, indicating the necessity of Nrf2 in the sesamol-mediated Ucp1 induction. Together, these findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expenditure, further highlighting the use of the Nrf2 activation in stimulating thermogenic adipocytes and in increasing energy expenditure in obesity and its related metabolic diseases.


greenmedinfo--2020-08-28--Sesamol protects testis from ischemia-reperfusion injury.

Testicular torsion/detorsion-induced damage is considered as a typical ischemia-reperfusion injury attributed to excessive reactive oxygen species ( ROS ) production .
ROS may regulate many genes whose expression affects cell-cycle regulation , cell proliferation , and apoptosis .
The cAMP-responsive element modulator- ( CREM ) gene expression in the testis is essential for normal germ cell differentiation .
The present study was aimed at investigating the effect of sesamol , a powerful antioxidant , on testicular ischemia-reperfusion injury and related mechanisms in an experimental testicular torsion-detorsion rat model .
The type of our study was a randomized controlled trial .
@ @ @ @ @ @ @ following 3 groups : ( 1 ) sham-operated control group ( = 20 ) , ( 2 ) testicular ischemia-reperfusion group ( = 20 ) , and ( 3 ) testicular ischemia-reperfusion+sesamol-treated group ( = 20 ) .
Testicular ischemia-reperfusion was induced by left testicular torsion ( 720° rotation in a counterclockwise direction ) for 2 hours , followed by detorsion .
Orchiectomy was performed at 4 hours or 3 months after detorsion .
The testis was obtained for the analysis of the following parameters , including malondialdehyde level ( a sensitive indicator @ @ @ @ @ @ @ spermatogenesis .
In the testicular ischemia-reperfusion group , the malondialdehyde level was significantly increased with a concomitant significant decrease in CREMexpression and spermatogenesis in ipsilateral testis .
These results suggest that overproduction of ROS after testicular ischemia-reperfusion may downregulate CREMexpression , which causes spermatogenic injury .
Sesamol treatment resulted in a significant reduction in the malondialdehyde level and significant increase in CREMexpression and spermatogenesis in ipsilateral testis .
These data support the above suggestion .
Our study shows that sesamol can attenuate testicular ischemia-reperfusion injury through scavenging ROS and upregulating CREMexpression .

Testicular torsion/detorsion-induced damage is considered as a typical ischemia-reperfusion injury attributed to excessive reactive oxygen species (ROS) production. ROS may regulate many genes whose expression affects cell-cycle regulation, cell proliferation, and apoptosis. The cAMP-responsive element modulator-(CREM) gene expression in the testis is essential for normal germ cell differentiation. The present study was aimed at investigating the effect of sesamol, a powerful antioxidant, on testicular ischemia-reperfusion injury and related mechanisms in an experimental testicular torsion-detorsion rat model. The type of our study was a randomized controlled trial. Sixty rats were randomly divided into the following 3 groups: (1) sham-operated control group (= 20), (2) testicular ischemia-reperfusion group (= 20), and (3) testicular ischemia-reperfusion+sesamol-treated group (= 20). Testicular ischemia-reperfusion was induced by left testicular torsion (720° rotation in a counterclockwise direction) for 2 hours, followed by detorsion. Orchiectomy was performed at 4 hours or 3 months after detorsion. The testis was obtained for the analysis of the following parameters, including malondialdehyde level (a sensitive indicator of ROS), CREMexpression, and spermatogenesis. In the testicular ischemia-reperfusion group, the malondialdehyde level was significantly increased with a concomitant significant decrease in CREMexpression and spermatogenesis in ipsilateral testis. These results suggest that overproduction of ROS after testicular ischemia-reperfusion may downregulate CREMexpression, which causes spermatogenic injury. Sesamol treatment resulted in a significant reduction in the malondialdehyde level and significant increase in CREMexpression and spermatogenesis in ipsilateral testis. These data support the above suggestion. Our study shows that sesamol can attenuate testicular ischemia-reperfusion injury through scavenging ROS and upregulating CREMexpression.


greenmedinfo--2020-08-28--Sesamum indicum oil and sesamin induce auditory-protective effects through changes in hearing loss-r

Sesamum indicum oil and sesamin induce auditory-protective effects through changes in hearing loss-related gene expression.

Changing consumption patterns and increasing health awareness , especially in Europe , are resulting in an increased demand for sesame seeds .
In 2016 , Asia imported the highest quantity of sesame seeds , followed by Europe and North America .
We examined , for the first time , the effects of treatment with sesame oil and sesamin in hearing impairment models .
Sesame oil exhibited an ameliorative effect on auditory impairment in a hair cell line in zebrafish and mice .
In ototoxic zebrafish larvae , neuromasts and otic cells increased in numbers because of sesame oil .
Furthermore @ @ @ @ @ @ @ ( NIHL ) was studied through auditory brainstem response to evaluate the therapeutic effects of sesame oil .
Sesame oil reduced the hearing threshold shift in response to clicks and 8 , 16-kHz tone bursts in NIHL mice .
Auditory-protective effect of sesame oil was seen in zebrafish and mice ; therefore , we used chromatographic analysis to study sesamin , which is the major effective factor in sesame oil .
To investigate its effects related to auditory function , we studied the hearing-related gene , , using the 3- ( 4,5-dimethylthiazol-2-yl ) @ @ @ @ @ @ @ cell proliferation was induced by treatment with sesame oil and sesamin using ( Tectorin Alpha ) regulation .
The expression ofincreases in the apex area of the cochlear hair cells as they grow , and their activity is enhanced by sesame oil and sesamin .
These results provide a novel mechanistic insight into the sesame oil activities and suggest that sesamin , the key constituent in sesame oil , is responsible for its auditory function related benefits , including protection of auditory cells and reversal of their impairments .

Changing consumption patterns and increasing health awareness, especially in Europe, are resulting in an increased demand for sesame seeds. In 2016, Asia imported the highest quantity of sesame seeds, followed by Europe and North America. We examined, for the first time, the effects of treatment with sesame oil and sesamin in hearing impairment models. Sesame oil exhibited an ameliorative effect on auditory impairment in a hair cell line in zebrafish and mice. In ototoxic zebrafish larvae, neuromasts and otic cells increased in numbers because of sesame oil. Furthermore, auditory function in noise-induced hearing loss (NIHL) was studied through auditory brainstem response to evaluate the therapeutic effects of sesame oil. Sesame oil reduced the hearing threshold shift in response to clicks and 8, 16-kHz tone bursts in NIHL mice. Auditory-protective effect of sesame oil was seen in zebrafish and mice; therefore, we used chromatographic analysis to study sesamin, which is the major effective factor in sesame oil. To investigate its effects related to auditory function, we studied the hearing-related gene,, using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT) assay. Auditory cell proliferation was induced by treatment with sesame oil and sesamin using(Tectorin Alpha) regulation. The expression ofincreases in the apex area of the cochlear hair cells as they grow, and their activity is enhanced by sesame oil and sesamin. These results provide a novel mechanistic insight into the sesame oil activities and suggest that sesamin, the key constituent in sesame oil, is responsible for its auditory function related benefits, including protection of auditory cells and reversal of their impairments.


greenmedinfo--2020-08-28--Sesamin promotes neurite outgrowth under insufficient nerve growth factor condition in PC12 cells.

The promotion of neurogenesis can be a promising strategy to improve and restore neuronal function in neurodegenerative diseases .
Nerve growth factor ( NGF ) plays a key role in neurite outgrowth and synaptic formation during brain repair stage .
Nowadays , there are several studies on the developing methods to enhance the endogenous NGF activity for treatment and restore the neuronal function .
In this study , the potentiating effect of sesamin , a major lignan in sesame seeds ( ) and oil , on NGF-induced neurogenesis and its involved mechanisms were firstly reported .
Sesamin effectively enhanced the @ @ @ @ @ @ @ under insufficient conditions of NGF .
The neuronal markers including synaptophysin and growth-associated protein-43 along with the synaptic connections were significantly increased in combination treatment between sesamin and NGF .
Moreover , sesamin also increased the level of phospho-ERK1/2 and SIRT1 protein , an important regulatory protein of the neurogenesis process .
The neurogenesis was blocked by the specific SIRT1 inhibitor , JGB1741 , suggesting that the neuritogenic effect of sesamin was associated with SIRT1 protein modulation .
Taken together , the potentiating effect of sesamin on NGF-induced neurogenesis in this finding could @ @ @ @ @ @ @ diseases , including Alzheimer 's disease .

The promotion of neurogenesis can be a promising strategy to improve and restore neuronal function in neurodegenerative diseases. Nerve growth factor (NGF) plays a key role in neurite outgrowth and synaptic formation during brain repair stage. Nowadays, there are several studies on the developing methods to enhance the endogenous NGF activity for treatment and restore the neuronal function. In this study, the potentiating effect of sesamin, a major lignan in sesame seeds () and oil, on NGF-induced neurogenesis and its involved mechanisms were firstly reported. Sesamin effectively enhanced the PC12 neuron-like cell differentiation and neurite length under insufficient conditions of NGF. The neuronal markers including synaptophysin and growth-associated protein-43 along with the synaptic connections were significantly increased in combination treatment between sesamin and NGF. Moreover, sesamin also increased the level of phospho-ERK1/2 and SIRT1 protein, an important regulatory protein of the neurogenesis process. The neurogenesis was blocked by the specific SIRT1 inhibitor, JGB1741, suggesting that the neuritogenic effect of sesamin was associated with SIRT1 protein modulation. Taken together, the potentiating effect of sesamin on NGF-induced neurogenesis in this finding could be used for alternative treatment in neurodegenerative diseases, including Alzheimer's disease.


greenmedinfo--2020-08-28--These results suggest that sesamolin induces apoptosis in HCT116 cells.

Colorectal cancer ( CRC ) is a common malignant tumor that seriously threatens human health and quality of life .
At present , the search for safe and more effective treatment for CRC has become necessary .
The present study investigated the anti-proliferative and apoptotic effects of sesamolin on human colorectal cancer ( HCT116 ) cells , and the underlying mechanism .
Cell proliferation was determined using MTT assay , while the expressions of JAK2 , STAT3 and p-STA3 were determined using Western blotting .
The levels of expression of matrix metalloproteinases-1 , 2 and 9 ( MMP1 , MMP2 @ @ @ @ @ @ @ quantitative polymerase chain reaction ( qRT-PCR ) .
The degree of migration and invasion of the cells was assessed using wound healing assay .
The results of MTT assay showed that sesamolin significantly and time- and dose-dependently inhibited the proliferation of HCT116 cells ( p < 0.05 ) .
Treatment of HCT116 cells with sesamolin significantly inhibited their migratory ability ( p < 0.05 ) .
The expressions of p-JAK2 and p-STAT3 were significantly down-regulated 48 h after 20µM of JAK2 specific inhibitor ( AG490 ) was added to HCT116 cells ( p @ @ @ @ @ @ @ p-STAT3 was also significantly and dose-dependently down-regulated 6 h after treatment of HCT116 cells with sesamolin ( p < 0.05 ) .
Sesamolin and AG490 had synergistic effect and their combination significantly down-regulated the expression of p-STAT3 , when compared with sesamolin alone ( p < 0.05 ) .
Treatment of HCT116 cells with sesamolin significantly and dose-dependently reduced the levels of IL-6-induced expressions of MMP-1 , MMP-2 and MMP-9 ( p < 0.05 ) .
These results suggest that sesamolin induces apoptosis in HCT116 cells and prevents cell invasion via inhibition of @ @ @ @ @

Colorectal cancer (CRC) is a common malignant tumor that seriously threatens human health and quality of life. At present, the search for safe and more effective treatment for CRC has become necessary. The present study investigated the anti-proliferative and apoptotic effects of sesamolin on human colorectal cancer (HCT116) cells, and the underlying mechanism. Cell proliferation was determined using MTT assay, while the expressions of JAK2, STAT3 and p-STA3 were determined using Western blotting. The levels of expression of matrix metalloproteinases-1, 2 and 9 (MMP1, MMP2 and MMP9) were determined using real-time quantitative polymerase chain reaction (qRT-PCR). The degree of migration and invasion of the cells was assessed using wound healing assay. The results of MTT assay showed that sesamolin significantly and time- and dose-dependently inhibited the proliferation of HCT116 cells (p< 0.05). Treatment of HCT116 cells with sesamolin significantly inhibited their migratory ability (p< 0.05). The expressions of p-JAK2 and p-STAT3 were significantly down-regulated 48 h after 20µM of JAK2 specific inhibitor (AG490) was added to HCT116 cells (p< 0.05). The expression of p-STAT3 was also significantly and dose-dependently down-regulated 6 h after treatment of HCT116 cells with sesamolin (p< 0.05). Sesamolin and AG490 had synergistic effect and their combination significantly down-regulated the expression of p-STAT3, when compared with sesamolin alone (p< 0.05). Treatment of HCT116 cells with sesamolin significantly and dose-dependently reduced the levels of IL-6-induced expressions of MMP-1, MMP-2 and MMP-9 (p< 0.05). These results suggest that sesamolin induces apoptosis in HCT116 cells and prevents cell invasion via inhibition of the JAK2/STAT3 signaling pathway.


greenmedinfo--2020-08-28--Sesamolin promotes cytolysis and migration activity of natural killer cells via dendritic cells.

The defense mechanism of the immune system is based on the interaction of many kinds of leukocytes .
Among them @ @ @ @ @ ) control most immune responses .
In our previous study , sesamolin was shown to @ @ @ @ @ natural killer ( NK ) cells to kill cancer cells .
Here we attempted to @ @ @ @ @ to promote the killing and migration activity of NK cells .
We co-cultured DCs and @ @ @ @ @ communication between them .
NK cells co-cultured with 5µg/ml sesamolin-treated mature dendritic cells ( mDCs @ @ @ @ @ than did NK cells or mDCs co-cultured NK cells .
Moreover , the migration of @ @ @ @ @ enhanced compared to immature dendritic cells ( iDCs ) .
The migration of NK cells @ @ @ @ @ after sesamolin activation of the mDCs .
Altogether , this study demonstrated that sesamolin activated @ @ @ @ @ differentiation and activation of DCs .

The defense mechanism of the immune system is based on the interaction of many kinds of leukocytes. Among them, dendritic cells (DCs) control most immune responses. In our previous study, sesamolin was shown to create an optimal environment for natural killer (NK) cells to kill cancer cells. Here we attempted to demonstrate how sesamolin influences DCs to promote the killing and migration activity of NK cells. We co-cultured DCs and NK cells and analyzed the communication between them. NK cells co-cultured with 5µg/ml sesamolin-treated mature dendritic cells (mDCs) had better cytolytic activity than did NK cells or mDCs co-cultured NK cells. Moreover, the migration of NK cells toward mDCs was enhanced compared to immature dendritic cells (iDCs). The migration of NK cells stimulated by mDCs was stronger after sesamolin activation of the mDCs. Altogether, this study demonstrated that sesamolin activated NK cells by modulating the differentiation and activation of DCs.


greenmedinfo--2020-08-28--Sesamin induces A549 cell mitophagy and mitochondrial apoptosis via a reactive oxygen species-mediat

Sesamin induces A549 cell mitophagy and mitochondrial apoptosis via a reactive oxygen species-mediated reduction in mitochondrial membrane potential.

Sesamin , a lipid-soluble lignin originally isolated from sesame seeds , which induces cancer cell apoptosis and autophagy .
In the present study , has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells .
However , whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear .
This study , the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species ( ROS ) and mitophagy .
A549 cells were treated with sesamin , and cell viability , migration ability , and cell cycle were assessed using the @ @ @ @ @ @ @ flow cytometry , respectively .
ROS levels , mitochondrial membrane potential , and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays .
The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G/Gphase arrest .
Furthermore , sesamin induced an increase in ROS levels , a reduction in mitochondrial membrane potential , and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9 .
Additionally , sesamin triggered mitophagy and increased the expression of PINK1 @ @ @ @ @ @ @ to the mitochondria .
However , the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin .
Furthermore , we found that cyclosporine A ( an inhibitor of mitophagy ) decreased the inhibitory effect of sesamin on A549 cell viability .
Collectively , our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis .

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G/Gphase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.


greenmedinfo--2020-08-28--Antimetastatic effects of sesamin on human head and neck squamous cell carcinoma.

BACKGROUND : Sesamin is a lignin present in sesame oil from the bark ofspp .
Sesamin reportedly has anticarcinogenic potential and exerts anti-inflammatory effects on several tumors .
Hypothesis/Purpose : However , the effect of sesamin on metastatic progression in human head and neck squamous carcinoma ( HNSCC ) remains unknown in vitro and in vivo ; hence , we investigated the effect of sesamin on HNSCC cells in vitro .
METHODS AND RESULTS : Sesamin-treated human oral cancer cell lines FaDu , HSC-3 , and Ca9-22 were subjected to a wound-healing assay .
Furthermore , Western blotting was performed @ @ @ @ @ @ @ the expression levels of matrix metalloproteinase ( MMP ) -2 and proteins of the MAPK signaling pathway , including p-ERK1/2 , P-p38 , and p-JNK1/2 .
In addition , we investigated the association between MMP-2 expression and the MAPK pathway in sesamin-treated oral cancer cells .
Sesamin inhibited cell migration and invasion in FaDu , Ca9-22 , and HSC-3 cells and suppressed MMP-2 at noncytotoxic concentrations ( 0 to 40μM ) .
Furthermore , sesamin significantly reduced p38 MAPK and JNK phosphorylation in a dose-dependent manner in FaDu and HSC-3 cells .
CONCLUSIONS @ @ @ @ @ @ @ the migration and invasion of HNSCC cells by regulating MMP-2 and is thus a potential antimetastatic agent for treating HNSCC .

BACKGROUND: Sesamin is a lignin present in sesame oil from the bark ofspp. Sesamin reportedly has anticarcinogenic potential and exerts anti-inflammatory effects on several tumors. Hypothesis/Purpose: However, the effect of sesamin on metastatic progression in human head and neck squamous carcinoma (HNSCC) remains unknown in vitro and in vivo; hence, we investigated the effect of sesamin on HNSCC cells in vitro.
METHODS AND RESULTS: Sesamin-treated human oral cancer cell lines FaDu, HSC-3, and Ca9-22 were subjected to a wound-healing assay. Furthermore, Western blotting was performed to assess the effect of sesamin on the expression levels of matrix metalloproteinase (MMP)-2 and proteins of the MAPK signaling pathway, including p-ERK1/2, P-p38, and p-JNK1/2. In addition, we investigated the association between MMP-2 expression and the MAPK pathway in sesamin-treated oral cancer cells. Sesamin inhibited cell migration and invasion in FaDu, Ca9-22, and HSC-3 cells and suppressed MMP-2 at noncytotoxic concentrations (0 to 40μM). Furthermore, sesamin significantly reduced p38 MAPK and JNK phosphorylation in a dose-dependent manner in FaDu and HSC-3 cells.
CONCLUSIONS: These results indicate that sesamin suppresses the migration and invasion of HNSCC cells by regulating MMP-2 and is thus a potential antimetastatic agent for treating HNSCC.


greenmedinfo--2020-08-28--Identification of a natural compound, sesamin, as a novel TRPM8 antagonist with inhibitory effects o

Identification of a natural compound, sesamin, as a novel TRPM8 antagonist with inhibitory effects on prostate adenocarcinoma

Transient receptor potential melastatin 8 ( TRPM8 ) is a calcium ion-permeable cation channel that is used as a prognostic marker and therapeutic target for different tumor types .
To identify natural selective TRPM8 antagonists , we tested 158 traditional Chinese medicine ( TCM ) compounds for the ability to inhibit TRPM8 .
Calcium mobilization assays were used to evaluate the 158 TCM compound components in HEK293 cells stably expressing TRPM8 .
An identified putative TRPM8 antagonist , sesamin , was further evaluated .
Publicly available cancer OMICS data were used to explore the expression of TRPM8 , its gene @ @ @ @ @ @ @ patients with prostate adenocarcinoma ( PRAD ) .
The cytotoxicity and specificity of sesamin to TRPM8 were tested in HEK293/TRPM8 cells .
The effect of sesamin on cell proliferation in PRAD cell lines was assessed .
Sesamin selectively inhibited TRPM8 in HEK293/TRPM8 cells ( IC50 : 9.78 μM ) , and a molecular docking study confirmed the binding of sesamin to TRPM8 .
TRPM8 was highly overexpressed in PRAD , and high TRPM8 expression was associated with poor survival of PRAD patients .
Functional network analysis suggested that TRPM8 has key effects on @ @ @ @ @ @ @ prostate cancer cells .
Cell proliferation assays supported these findings and showed that sesamin inhibited the proliferation of PRAD cell lines DU145 and LNCaP cells .
These data revealed that abnormal TRPM8 expression is associated with PRAD and that sesamin is a new anti-PRAD candidate drug , exerting inhibitory effects on TRPM8 .

Transient receptor potential melastatin 8 (TRPM8) is a calcium ion-permeable cation channel that is used as a prognostic marker and therapeutic target for different tumor types. To identify natural selective TRPM8 antagonists, we tested 158 traditional Chinese medicine (TCM) compounds for the ability to inhibit TRPM8. Calcium mobilization assays were used to evaluate the 158 TCM compound components in HEK293 cells stably expressing TRPM8. An identified putative TRPM8 antagonist, sesamin, was further evaluated. Publicly available cancer OMICS data were used to explore the expression of TRPM8, its gene regulatory network, and the survival of patients with prostate adenocarcinoma (PRAD). The cytotoxicity and specificity of sesamin to TRPM8 were tested in HEK293/TRPM8 cells. The effect of sesamin on cell proliferation in PRAD cell lines was assessed. Sesamin selectively inhibited TRPM8 in HEK293/TRPM8 cells (IC50: 9.78 μM), and a molecular docking study confirmed the binding of sesamin to TRPM8. TRPM8 was highly overexpressed in PRAD, and high TRPM8 expression was associated with poor survival of PRAD patients. Functional network analysis suggested that TRPM8 has key effects on proliferation, survival, and invasion of prostate cancer cells. Cell proliferation assays supported these findings and showed that sesamin inhibited the proliferation of PRAD cell lines DU145 and LNCaP cells. These data revealed that abnormal TRPM8 expression is associated with PRAD and that sesamin is a new anti-PRAD candidate drug, exerting inhibitory effects on TRPM8.


greenmedinfo--2020-08-28--Sesame lignans suppress age-related disorders of the kidney in mice.

OBJECTIVE : Sesamin is a functional ingredient in sesame ( Sesamum indicum ) seeds and has many physiological effects .
This study investigated whether sesame lignans , sesamin and episesamin ( 1:1 ) , can suppress age-related disorders of the kidney .
MATERIALS AND METHODS : Twenty-month-old mice were divided into three groups , and each group received a regular diet ( O-C ) , diet containing sesame lignans ( O-SE ) , and diet containing sesame lignans andα-tocopherol ( VE ; O-SE+VE ) , respectively , for 5 months .
Six-month-old young mice ( Y-C ) were compared to @ @ @ @ @ @ @ lipofuscin deposition was increased in the O-C group compared to that in the Y-C group and its deposition with aging was significantly decreased in both O-SE and O-SE+VE groups .
Plasma blood urea nitrogen levels in the O-C group increased compared to those in the Y-C group ; however , those in both O-SE and O-SE+VE groups did not differ from those in the Y-C group .
The number of podocytes in the O-C group decreased compared to that in the Y-C group and this effect was attenuated in the O-SE and O-SE+VE @ @ @ @ @ @ @ the O-SE+VE group .
Histological examinations showed that glomerular hypertrophy accompanied by mesangial hyperplasia and renal tubular degeneration was less severe in the O-SE and O-SE+VE groups than in the O-C group .
Moreover , age-related increases in the mRNA expression of NADPH oxidase- and inflammation-related genes , including p67phox , p40phox , TNFα , and IL-6 , in the kidney were suppressed in the O-SE and O-SE+VE groups .
CONCLUSIONS : Sesame lignans might be useful to suppress age-related kidney disorders , and these effects could be enhanced with VE .

OBJECTIVE: Sesamin is a functional ingredient in sesame (Sesamum indicum) seeds and has many physiological effects. This study investigated whether sesame lignans, sesamin and episesamin (1:1), can suppress age-related disorders of the kidney.
MATERIALS AND METHODS: Twenty-month-old mice were divided into three groups, and each group received a regular diet (O-C), diet containing sesame lignans (O-SE), and diet containing sesame lignans andα-tocopherol (VE; O-SE+VE), respectively, for 5 months. Six-month-old young mice (Y-C) were compared to the older mice.
RESULTS: Renal lipofuscin deposition was increased in the O-C group compared to that in the Y-C group and its deposition with aging was significantly decreased in both O-SE and O-SE+VE groups. Plasma blood urea nitrogen levels in the O-C group increased compared to those in the Y-C group; however, those in both O-SE and O-SE+VE groups did not differ from those in the Y-C group. The number of podocytes in the O-C group decreased compared to that in the Y-C group and this effect was attenuated in the O-SE and O-SE+VE groups. The effect was strongest in the O-SE+VE group. Histological examinations showed that glomerular hypertrophy accompanied by mesangial hyperplasia and renal tubular degeneration was less severe in the O-SE and O-SE+VE groups than in the O-C group. Moreover, age-related increases in the mRNA expression of NADPH oxidase- and inflammation-related genes, including p67phox, p40phox, TNFα, and IL-6, in the kidney were suppressed in the O-SE and O-SE+VE groups.
CONCLUSIONS: Sesame lignans might be useful to suppress age-related kidney disorders, and these effects could be enhanced with VE.


greenmedinfo--2020-08-28--Inhibition of programmed death ligand 1 (PD-L1) expression in breast cancer cells by sesamin.

Programmed death ligand 1 ( PD-L1 ) is overexpressed in some metastatic breast cancer subtypes , specifically triple-negative breast cancer ( TNBC ) .
This feature can assist in the eradication of anti-tumor immunity , thereby enhancing the survival of the tumor .
This study aims to explore how sesamin affects PD-L1 expression in breast cancer cells and its related molecular mechanisms .
We found high levels of expression of PD-L1 in both mRNA and protein levels in the TNBC cell line , MDA-MB231 , but not in the luminal type-breast cancer cell line , MCF-7 .
We then demonstrated @ @ @ @ @ @ @ which induced the inhibition of cell proliferation in MDA-MB231 cells .
Additionally , sesamin triggered PD-L1 downregulation ( both mRNA and protein ) through the inhibition of AKT , NF-κB and JAK/Stat signaling in MDA-MB231 cells .
Moreover , the migration ability of MDA-MB231 cells was effectively diminished by sesamin via inhibition of the activation of MMP-9 and MMP-2 .
In summary , this study demonstrated that sesamin suppresses MDA-MB231 breast cancer cells ' proliferation and migration ; and decreases the expression of PD-L1 via the downregulation of AKT , NF-κB , and @ @ @ @ @ @ @ be an effective alternative and novel therapeutic option for immunotherapy in breast cancer cells with high PD-L1 expression .

Programmed death ligand 1 (PD-L1) is overexpressed in some metastatic breast cancer subtypes, specifically triple-negative breast cancer (TNBC). This feature can assist in the eradication of anti-tumor immunity, thereby enhancing the survival of the tumor. This study aims to explore how sesamin affects PD-L1 expression in breast cancer cells and its related molecular mechanisms. We found high levels of expression of PD-L1 in both mRNA and protein levels in the TNBC cell line, MDA-MB231, but not in the luminal type-breast cancer cell line, MCF-7. We then demonstrated the tumor suppressive effect of sesamin, which induced the inhibition of cell proliferation in MDA-MB231 cells. Additionally, sesamin triggered PD-L1 downregulation (both mRNA and protein) through the inhibition of AKT, NF-κB and JAK/Stat signaling in MDA-MB231 cells. Moreover, the migration ability of MDA-MB231 cells was effectively diminished by sesamin via inhibition of the activation of MMP-9 and MMP-2. In summary, this study demonstrated that sesamin suppresses MDA-MB231 breast cancer cells' proliferation and migration; and decreases the expression of PD-L1 via the downregulation of AKT, NF-κB, and JAK/Stat signaling. Therefore, sesamin may be an effective alternative and novel therapeutic option for immunotherapy in breast cancer cells with high PD-L1 expression.


greenmedinfo--2020-08-28--Effects of sesamin on fatty acid and cholesterol metabolism, macrophage cholesterol homeostasis and

Effects of sesamin on fatty acid and cholesterol metabolism, macrophage cholesterol homeostasis and serum lipid profile.

Sesamin is the major lignan constituent derived from Sesamum indicum seeds and sesame oil .
Various studies have reported that sesamin possesses potent lipid-lowering properties .
The lipid-lowering effects of sesamin have been mainly attributed to its ability in affecting key events in fatty acid and cholesterol metabolism and in lowering atherogenesis-triggering LDL , VLDL and TG levels , as well as in increasing atheroprotective HDL levels .
In this review , we provide a comprehensive summary of the reported anti-hyperlipidemic effects of sesamin , presented both in vitro and in vivo .
The molecular anti-hyperlipidemic properties of sesamin that @ @ @ @ @ @ @ discussed and analyzed .
Studies focusing on the ability of sesamin to inhibit fatty acid synthesis , induce fatty acid oxidation , inhibit cholesterol synthesis and absorption and maintain macrophage cholesterol homeostasis are outlined .
The effects of sesamin on circulating serum and liver lipid levels are also highlighted .
Moreover , the anti-hyperlipidemic effects of sesamin are compared to those of other important sesame lignans like sesamolin and episesamin .
Findings reveal that sesamin mainly exerts its anti-hyperlipidemic effects by targetingΔ5 desaturase , HMGCR , ABCA1 and ABCG1 through PPARα , PPARγ @ @ @ @ @ @ @ .
Overall , the amount of evidence supporting the anti-hyperlipidemic potential of sesamin in vitro and in vivo is compelling .
A thorough understanding of the mechanisms underlying the anti-hyperlipidemic properties of sesamin is imperative for the possible employment of sesamin as an anti-hyperlipidemic and anti-atherogenic agent with minimal side effects .

Sesamin is the major lignan constituent derived from Sesamum indicum seeds and sesame oil. Various studies have reported that sesamin possesses potent lipid-lowering properties. The lipid-lowering effects of sesamin have been mainly attributed to its ability in affecting key events in fatty acid and cholesterol metabolism and in lowering atherogenesis-triggering LDL, VLDL and TG levels, as well as in increasing atheroprotective HDL levels. In this review, we provide a comprehensive summary of the reported anti-hyperlipidemic effects of sesamin, presented both in vitro and in vivo. The molecular anti-hyperlipidemic properties of sesamin that underlie its well-documented anti-atherogenic effects are thoroughly discussed and analyzed. Studies focusing on the ability of sesamin to inhibit fatty acid synthesis, induce fatty acid oxidation, inhibit cholesterol synthesis and absorption and maintain macrophage cholesterol homeostasis are outlined. The effects of sesamin on circulating serum and liver lipid levels are also highlighted. Moreover, the anti-hyperlipidemic effects of sesamin are compared to those of other important sesame lignans like sesamolin and episesamin. Findings reveal that sesamin mainly exerts its anti-hyperlipidemic effects by targetingΔ5 desaturase, HMGCR, ABCA1 and ABCG1 through PPARα, PPARγ, LXRα, and SREBP signaling pathways. Overall, the amount of evidence supporting the anti-hyperlipidemic potential of sesamin in vitro and in vivo is compelling. A thorough understanding of the mechanisms underlying the anti-hyperlipidemic properties of sesamin is imperative for the possible employment of sesamin as an anti-hyperlipidemic and anti-atherogenic agent with minimal side effects.


greenmedinfo--2020-08-28--This study demonstrated an antiasthmatic effect of Bilsaan through the modulation of Th2 immune resp

This study demonstrated an antiasthmatic effect of Bilsaan through the modulation of Th2 immune responses, inflammation, and the oxidative stress.

Asthma is characterized by the elevated level of Th2 immune responses , oxidative stress , and airway inflammation .
Bilsaan , an exudate from the stem of , has been traditionally used in the treatment of various ailments in Saudi Arabia .
Here , we investigated the therapeutic potential of Bilsaan against ovalbumin- ( OVA- ) induced allergic asthma in a mouse model .
In order to induce allergic asthma , mice were intraperitoneally injected with alum-emulsified-OVA ( 20 g/mouse ) on days 0 , 14 , and 21 that is followed by an intranasal OVA exposure from days 22 @ @ @ @ @ @ @ mice were orally administered with Bilsaan at the doses of 5 , 10 , and 25 mg/kg .
The numbers of total and differential inflammatory cells and the levels of Th2 cytokines ( IL-4 , IL-5 , and IL-13 ) and IgE were determined in bronchoalveolar lavage fluid ( BALF ) .
Moreover , the therapeutic effect of Bilsaan was also assessed to analyze the oxidative stress and inflammatory changes in the lung tissues .
The results demonstrated that Bilsaan treatment significantly reduced the total and differential inflammatory cell count in the BALF @ @ @ @ @ @ @ with Bilsaan showed significantly lower levels of IL-4 , IL-5 , IL-13 , and IgE .
Interestingly , a similar pattern was observed in IL-4 , IL-5 , and IL-13 secreted by OVA-sensitized splenocytes from the mice of various groups .
Bilsaan treatment alleviated the status of oxidative stress by modulating malondialdehyde ( MDA ) , superoxide dismutase ( SOD ) , and catalase levels in the lung .
Moreover , Bilsaan treatment reduced the infiltration of inflammatory cells , thickening of alveolar wall , and congestion in the lung tissues .
The @ @ @ @ @ @ @ antiasthmatic effect of Bilsaan through the modulation of Th2 immune responses , inflammation , and the oxidative stress .

Asthma is characterized by the elevated level of Th2 immune responses, oxidative stress, and airway inflammation. Bilsaan, an exudate from the stem of, has been traditionally used in the treatment of various ailments in Saudi Arabia. Here, we investigated the therapeutic potential of Bilsaan against ovalbumin- (OVA-) induced allergic asthma in a mouse model. In order to induce allergic asthma, mice were intraperitoneally injected with alum-emulsified-OVA (20 g/mouse) on days 0, 14, and 21 that is followed by an intranasal OVA exposure from days 22 to 30. During this time, mice were orally administered with Bilsaan at the doses of 5, 10, and 25 mg/kg. The numbers of total and differential inflammatory cells and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) and IgE were determined in bronchoalveolar lavage fluid (BALF). Moreover, the therapeutic effect of Bilsaan was also assessed to analyze the oxidative stress and inflammatory changes in the lung tissues. The results demonstrated that Bilsaan treatment significantly reduced the total and differential inflammatory cell count in the BALF. The BALF from the mice treated with Bilsaan showed significantly lower levels of IL-4, IL-5, IL-13, and IgE. Interestingly, a similar pattern was observed in IL-4, IL-5, and IL-13 secreted by OVA-sensitized splenocytes from the mice of various groups. Bilsaan treatment alleviated the status of oxidative stress by modulating malondialdehyde (MDA), superoxide dismutase (SOD), and catalase levels in the lung. Moreover, Bilsaan treatment reduced the infiltration of inflammatory cells, thickening of alveolar wall, and congestion in the lung tissues. The findings of the present study demonstrated an antiasthmatic effect of Bilsaan through the modulation of Th2 immune responses, inflammation, and the oxidative stress.


greenmedinfo--2020-08-28--Methylsulfonylmethane exhibits bacteriostatic inhibition of Escherichia coli, and Salmonella enteric

Methylsulfonylmethane exhibits bacteriostatic inhibition of Escherichia coli, and Salmonella enterica Kinshasa.

AIMS : To evaluate antibacterial properties of methylsulfonylmethane ( MSM ) on Escherichia coli ( MDRE21 ) and Salmonella enterica serovar Kinshasa ( SK132 ) .
METHODS AND RESULTS : Bacterial proliferation analysis was measured spectrophotometrically during log phase growth with 0 , 3 , 5 , 7 , 10 , 12 and 16 % MSM .
To assess the mechanism of inhibition , cultures were grown overnight with 0-16 % MSM and enumerated on unmedicated brain-heart infusion agar ( BHIA ) or BHIA with 0-16 % MSM .
The long-term viability studies were done to evaluate the impact of @ @ @ @ @ @ @ a dose-dependent inhibition from 0 to 16 % MSM .
There was no growth of MDRE21 or SK132 on BHIA in 10-16 % MSM .
Both strains enumerated on unmedicated BHIA from overnight cultures with 10-16 % MSM were able to partially recover .
CONCLUSIONS : Recovery after MSM removal may be indicative of a bacteriostatic mechanism of inhibition .
The long-term viability studies illustrated that neither MDRE21 nor SK132 could be rescued from 10 % MSM after 5 or 6 days respectively .
SIGNIFICANCE AND IMPACT OF THE STUDY : Methylsulfonylmethane antibacterial @ @ @ @ @ @ @ postharvest food safety as a disinfectant .
The primary benefit being , its clinical safety to humans .
Comparisons to other disinfectants would also need to be done to determine if MSM was superior to those already on the market and would be cost effective .

AIMS: To evaluate antibacterial properties of methylsulfonylmethane (MSM) on Escherichia coli (MDRE21) and Salmonella enterica serovar Kinshasa (SK132).
METHODS AND RESULTS: Bacterial proliferation analysis was measured spectrophotometrically during log phase growth with 0, 3, 5, 7, 10, 12 and 16% MSM. To assess the mechanism of inhibition, cultures were grown overnight with 0-16% MSM and enumerated on unmedicated brain-heart infusion agar (BHIA) or BHIA with 0-16% MSM. The long-term viability studies were done to evaluate the impact of 10% MSM. Absorbance data indicated a dose-dependent inhibition from 0 to 16% MSM. There was no growth of MDRE21 or SK132 on BHIA in 10-16% MSM. Both strains enumerated on unmedicated BHIA from overnight cultures with 10-16% MSM were able to partially recover.
CONCLUSIONS: Recovery after MSM removal may be indicative of a bacteriostatic mechanism of inhibition. The long-term viability studies illustrated that neither MDRE21 nor SK132 could be rescued from 10% MSM after 5 or 6 days respectively.
SIGNIFICANCE AND IMPACT OF THE STUDY: Methylsulfonylmethane antibacterial activity may prove useful during pre or postharvest food safety as a disinfectant. The primary benefit being, its clinical safety to humans. Comparisons to other disinfectants would also need to be done to determine if MSM was superior to those already on the market and would be cost effective.


greenmedinfo--2020-08-28--Consumption of pomegranate peel extract in combination with vitamin E enhanced the inflammatory stat

Consumption of pomegranate peel extract in combination with vitamin E enhanced the inflammatory status and endothelial function in hemodialysis patients.

Inflammation and endothelial dysfunction are major problems in hemodialysis ( HD ) patients .
This study assessed the effects of an 8 week administration of pomegranate peel extract ( PPE ) and vitamin E ( Vit E ) alone or in combination on the biomarkers of inflammation , including C-reactive protein ( CRP ) , interleukin-6 ( IL-6 ) , and tumor necrosis factor-alpha ( TNF-α ) , and the biomarkers of endothelial function , including intercellular adhesion molecule-1 ( ICAM-1 ) , vascular cell adhesion molecule-1 ( VCAM-1 ) , and P-selectin , in HD patients .
In a @ @ @ @ @ @ @ trial , 100 HD patients were randomly divided into 4 equal groups : ( a ) PPE + Vit E , received 2 pomegranate tablets ( each tablet contained 225 mg PPE , equal to 90 mg ellagic acid ) + 1 Vit E soft gel ( 400 IU ) daily , ( b ) PPE , received 2 pomegranate tablets + 1 Vit E placebo soft gel daily , ( c ) Vit E , received 1 Vit E soft gel + 2 pomegranate placebo tablets daily , and ( d ) @ @ @ @ @ @ @ + 1 Vit E placebo soft gel daily .
For group allocation , a stratified block randomization procedure based on sex , age , and HD duration was used .
Each intervention product and its placebo had identical shape , color , size , and packaging .
Consumption of PPE + Vit E significantly reduced the serum CRP level ( mean change : -7.12 ± 4.59 mg l-1 , P < 0.001 ) compared to other groups , while reduced levels of IL-6 ( mean change : -2.19± 2.33 pg ml-1 , P @ @ @ @ @ @ @ change : -2.41 ± 3.21 pg ml-1 , P = 0.008 ) , ICAM-1 ( mean change : -64.2 ± 111.0 ng ml-1 , P = 0.017 ) , and VCAM-1 ( mean change : -117.7 ± 177.1 ng ml-1 , P = 0.002 ) were observed compared to the control .
There was no significant difference in the P-selectin level among the groups .
Consumption of PPE or Vit E alone significantly reduced the CRP level ( mean change for PPE : -3.58 ± 5.41 mg l-1 , P < 0.001 ; @ @ @ @ @ @ @ 8.29 mg l-1 , P = 0.002 ) compared to the control .
As a result , consumption of PPE in combination with Vit E enhanced the inflammatory status and endothelial function in HD patients .

Inflammation and endothelial dysfunction are major problems in hemodialysis (HD) patients. This study assessed the effects of an 8 week administration of pomegranate peel extract (PPE) and vitamin E (Vit E) alone or in combination on the biomarkers of inflammation, including C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), and the biomarkers of endothelial function, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and P-selectin, in HD patients. In a randomized, double-blind, parallel, placebo-controlled trial, 100 HD patients were randomly divided into 4 equal groups: (a) PPE + Vit E, received 2 pomegranate tablets (each tablet contained 225 mg PPE, equal to 90 mg ellagic acid) + 1 Vit E soft gel (400 IU) daily, (b) PPE, received 2 pomegranate tablets + 1 Vit E placebo soft gel daily, (c) Vit E, received 1 Vit E soft gel + 2 pomegranate placebo tablets daily, and (d) placebo, received 2 pomegranate placebo tablets + 1 Vit E placebo soft gel daily. For group allocation, a stratified block randomization procedure based on sex, age, and HD duration was used. Each intervention product and its placebo had identical shape, color, size, and packaging. Consumption of PPE + Vit E significantly reduced the serum CRP level (mean change: -7.12 ± 4.59 mg l-1, P<0.001) compared to other groups, while reduced levels of IL-6 (mean change: -2.19± 2.33 pg ml-1, P<0.001), TNF-α (mean change: -2.41 ± 3.21 pg ml-1, P = 0.008), ICAM-1 (mean change: -64.2 ± 111.0 ng ml-1, P = 0.017), and VCAM-1 (mean change: -117.7 ± 177.1 ng ml-1, P = 0.002) were observed compared to the control. There was no significant difference in the P-selectin level among the groups. Consumption of PPE or Vit E alone significantly reduced the CRP level (mean change for PPE: -3.58 ± 5.41 mg l-1, P<0.001; mean change for Vit E: -3.25± 8.29 mg l-1, P = 0.002) compared to the control. As a result, consumption of PPE in combination with Vit E enhanced the inflammatory status and endothelial function in HD patients.


greenmedinfo--2020-08-28--Punicalagin in combination with zinc may promote certain anti-inflammatory and fibroblast responses

Punicalagin in combination with zinc may promote certain anti-inflammatory and fibroblast responses to aid oral healing.

Pomegranate ( ) is a well-established folklore medicine , demonstrating benefits in treating numerous conditions partly due to its antimicrobial and anti-inflammatory properties .
Such desirable medicinal capabilities are attributed to a high hydrolysable tannin content , especially punicalagin .
However , few studies have evaluated the abilities of pomegranate to promote oral healing , during situations such as periodontal disease or trauma .
Therefore , this study evaluated the antioxidant and in vitro gingival wound healing effects of pomegranate rind extract ( PRE ) and punicalagin , alone and in combination with Zn ( II ) .
In vitro @ @ @ @ @ @ @ ABTS assays , with total PRE phenolic content measured by Folin-Ciocalteu assay .
PRE , punicalagin and Zn ( II ) combination effects on human gingival fibroblast viability/proliferation and migration were investigated by MTT assay and scratch wounds , respectively .
Punicalagin demonstrated superior antioxidant capacities to PRE , although Zn ( II ) exerted no additional influences .
PRE , punicalagin and Zn ( II ) reduced gingival fibroblast viability and migration at high concentrations , but retained viability at lower concentrations without Zn ( II ) .
Fibroblast speed and distance @ @ @ @ @ @ @ punicalagin with Zn ( II ) at low concentrations .
Therefore , punicalagin in combination with Zn ( II ) may promote certain anti-inflammatory and fibroblast responses to aid oral healing .

Pomegranate () is a well-established folklore medicine, demonstrating benefits in treating numerous conditions partly due to its antimicrobial and anti-inflammatory properties. Such desirable medicinal capabilities are attributed to a high hydrolysable tannin content, especially punicalagin. However, few studies have evaluated the abilities of pomegranate to promote oral healing, during situations such as periodontal disease or trauma. Therefore, this study evaluated the antioxidant and in vitro gingival wound healing effects of pomegranate rind extract (PRE) and punicalagin, alone and in combination with Zn (II). In vitro antioxidant activities were studied using DPPH and ABTS assays, with total PRE phenolic content measured by Folin-Ciocalteu assay. PRE, punicalagin and Zn (II) combination effects on human gingival fibroblast viability/proliferation and migration were investigated by MTT assay and scratch wounds, respectively. Punicalagin demonstrated superior antioxidant capacities to PRE, although Zn (II) exerted no additional influences. PRE, punicalagin and Zn (II) reduced gingival fibroblast viability and migration at high concentrations, but retained viability at lower concentrations without Zn (II). Fibroblast speed and distance travelled during migration were also enhanced by punicalagin with Zn (II) at low concentrations. Therefore, punicalagin in combination with Zn (II) may promote certain anti-inflammatory and fibroblast responses to aid oral healing.


greenmedinfo--2020-08-28--Effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes.

Obesity is defined as a condition of excessive fat tissue accumulation .
It was the major factor most closely associated with lifestyle-related diseases .
In the present study , we investigated the effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes .
3T3-L1 adipocytes were treated with 0-25µg/mL of astaxanthin for 0-48 h. The result indicated that astaxanthin significantly decreased the oil Red O stained material ( OROSM ) , intracellular triglyceride accumulation , and glycerol 3-phosphate dehydrogenase ( GPDH ) activity in 3T3-L1 adipocytes ( < 0.05 ) .
At the molecular level , astaxanthin significantly @ @ @ @ @ @ @ in 3T3-L1 adipocytes ( < 0.05 ) .
Moreover , target genes ofon the inhibition of lipogenesis , such as ( ) , ( ) , ( ) , ( ) , and ( ) in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner ( < 0.05 ) .
These results suggested that astaxanthin efficiently suppressed lipid accumulation in 3T3-L1 adipocytes and its action is associated with the down-regulation of lipogenesis-related genes and the triglyceride accumulation in 3T3-L1 adipocytes .
Therefore , astaxanthin can be developed as a potential nutraceutical ingredient for @ @ @ @ @ @ @ market .

Obesity is defined as a condition of excessive fat tissue accumulation. It was the major factor most closely associated with lifestyle-related diseases. In the present study, we investigated the effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated with 0-25µg/mL of astaxanthin for 0-48 h. The result indicated that astaxanthin significantly decreased the oil Red O stained material (OROSM), intracellular triglyceride accumulation, and glycerol 3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes (<0.05). At the molecular level, astaxanthin significantly down-regulated the mRNA expression of() in 3T3-L1 adipocytes (<0.05). Moreover, target genes ofon the inhibition of lipogenesis, such as(),(),(),(), and() in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner (<0.05). These results suggested that astaxanthin efficiently suppressed lipid accumulation in 3T3-L1 adipocytes and its action is associated with the down-regulation of lipogenesis-related genes and the triglyceride accumulation in 3T3-L1 adipocytes. Therefore, astaxanthin can be developed as a potential nutraceutical ingredient for the prevention of obesity in a niche market.


greenmedinfo--2020-08-28--Anti-tumor effects of astaxanthin by inhibition of the expression of STAT3 in prostate cancer.

Astaxanthin is a natural product gaining increasing attention due to its safety and anti-cancer properties .
In this study , we investigated the mechanisms of the anti-cancer effects of astaxanthin on prostate cancer ( PCa ) cell lines using aggressive PCa DU145 cells .
Also an instantaneous silenced cell line ( si-STAT3 ) derived from DU145 and a control cell line ( si-NK ) were used for the MTT and colony formation assays to determine the role of astaxanthin in proliferation and colony formation abilities .
Flow cytometry assays were used to detect the apoptosis of tumor cells .
Migration @ @ @ @ @ @ @ the respective abilities .
Western blot and RT-PCR tests detected the levels of STAT3 protein and mRNA .
Astaxanthin resulted in suppression of the proliferation of DU145 cells and the level of STAT3 .
The treatment of DU145 cells with astaxanthin decreased the cloning ability , increased the apoptosis percentage and weakened the abilities of migration and invasion of the cells .
Furthermore , astaxanthin reduced the expression of STAT3 at protein and mRNA levels .
The effects were enhanced when astaxanthin and si-STAT3 were combined .
The results of animal experiments were @ @ @ @ @ @ @ Thus , astaxanthin inhibits the proliferation of DU145 cells by reducing the expression of STAT3 .

Astaxanthin is a natural product gaining increasing attention due to its safety and anti-cancer properties. In this study, we investigated the mechanisms of the anti-cancer effects of astaxanthin on prostate cancer (PCa) cell lines using aggressive PCa DU145 cells. Also an instantaneous silenced cell line (si-STAT3) derived from DU145 and a control cell line (si-NK) were used for the MTT and colony formation assays to determine the role of astaxanthin in proliferation and colony formation abilities. Flow cytometry assays were used to detect the apoptosis of tumor cells. Migration and invasion assays detected the weakening of the respective abilities. Western blot and RT-PCR tests detected the levels of STAT3 protein and mRNA. Astaxanthin resulted in suppression of the proliferation of DU145 cells and the level of STAT3. The treatment of DU145 cells with astaxanthin decreased the cloning ability, increased the apoptosis percentage and weakened the abilities of migration and invasion of the cells. Furthermore, astaxanthin reduced the expression of STAT3 at protein and mRNA levels. The effects were enhanced when astaxanthin and si-STAT3 were combined. The results of animal experiments were consistent with the results in cells. Thus, astaxanthin inhibits the proliferation of DU145 cells by reducing the expression of STAT3.


greenmedinfo--2020-08-28--Astaxanthin protects retinal photoreceptor cells against high glucose-induced oxidative stress.

Diabetic retinopathy ( DR ) is a major microvascular complication that can lead to severe visual impairment in patients with diabetes .
The elevated oxidative stress and increased reactive oxygen species ( ROS ) production induced by hyperglycemia have been reported to play an important role in the complex pathogenesis of DR. Astaxanthin ( AST ) , a natural carotenoid derivative , has been recently recognized as a strong free radical scavenger and might , therefore , be beneficial in different diseases , including DR .
In this study , we evaluated the potential role of AST as an antioxidative @ @ @ @ @ @ @ and also investigated the involvement of the PI3K/Akt/Nrf2 pathway in AST-mediated effects .
We treated high glucose-cultured mouse photoreceptor cells ( 661W ) with different concentrations of AST and analyzed ROS production and cell apoptosis in the different regimens .
Moreover , we also analyzed the expression of PI3K , Akt , Nrf2 , and Phase II enzymes after AST treatment .
Our results showed that AST dose-dependently reduced ROS production and attenuated 661W cell apoptosis in a high glucose environment .
Importantly , its protective effect was abolished by treatment with PI3K @ @ @ @ @ @ @ of the PI3K/Akt/Nrf2 pathway .
These results suggest AST as a nutritional supplement that could benefit patients with DR .

Diabetic retinopathy (DR) is a major microvascular complication that can lead to severe visual impairment in patients with diabetes. The elevated oxidative stress and increased reactive oxygen species (ROS) production induced by hyperglycemia have been reported to play an important role in the complex pathogenesis of DR. Astaxanthin (AST), a natural carotenoid derivative, has been recently recognized as a strong free radical scavenger and might, therefore, be beneficial in different diseases, including DR. In this study, we evaluated the potential role of AST as an antioxidative and antiapoptotic agent in protecting retinal cells and also investigated the involvement of the PI3K/Akt/Nrf2 pathway in AST-mediated effects. We treated high glucose-cultured mouse photoreceptor cells (661W) with different concentrations of AST and analyzed ROS production and cell apoptosis in the different regimens. Moreover, we also analyzed the expression of PI3K, Akt, Nrf2, and Phase II enzymes after AST treatment. Our results showed that AST dose-dependently reduced ROS production and attenuated 661W cell apoptosis in a high glucose environment. Importantly, its protective effect was abolished by treatment with PI3K or Nrf2 inhibitors, indicating the involvement of the PI3K/Akt/Nrf2 pathway. These results suggest AST as a nutritional supplement that could benefit patients with DR.


greenmedinfo--2020-08-28--Astaxanthin inhibits alcohol-induced inflammation and oxidative stress in macrophages.

OBJECTIVES : Alcohol induces inflammation and oxidative stress , causing cell damages .
We previously demonstrated that astaxanthin ( ASTX ) , a xanthophyll carotenoid , exerts anti-inflammatory and antioxidant properties in macrophages exposed to inflammatory insults .
In this study , we investigated whether ASTX can inhibit alcohol-induced inflammation and oxidative stress in macrophages with the elucidation of mechanisms .
METHODS : RAW 264.7 macrophages and mouse bone marrow-derived macrophages ( BMDM ) were treated with 80 mM ethanol in the presence or absence of 25μM of ASTX for 72 h. Subsequently , the expression of genes related to @ @ @ @ @ @ @ oxygen species ( ROS ) accumulation , cellular NADlevel , and SIRT1 activity were measured .
In addition , RAW 264.7 macrophages were treated with sirtinol or resveratrol , which are known inhibitor or activator of SIRT1 activity , respectively , to determine the contribution of SIRT1 to the inhibitory effect of ASTX on inflammation and oxidative stress in macrophages exposed to ethanol .
RESULTS : Ethanol increased mRNA expression of interleukin ( Il ) -6 , Il-1b , and tumor necrosis factorα with a concomitant increase in nuclear translocation of nuclear factor @ @ @ @ @ @ @ .
Importantly , ethanol significantly decreased SIRT1 activity and cellular NADlevel , but ASTX markedly attenuated the decreases in RAW 264.7 macrophages .
Sirtinol increased the expression of pro-inflammatory genes in ethanol-induced RAW 264.7 macrophages .
In contrast , resveratrol decreased pro-inflammatory gene expression .
CONCLUSIONS : ASTX showed anti-inflammatory and antioxidant properties by inhibiting decreases in SIRT1 expression and cellular NADlevel in ethanol-treated macrophages .
Therefore , ASTX may be used for the prevention of alcohol-induced cell damages .

OBJECTIVES: Alcohol induces inflammation and oxidative stress, causing cell damages. We previously demonstrated that astaxanthin (ASTX), a xanthophyll carotenoid, exerts anti-inflammatory and antioxidant properties in macrophages exposed to inflammatory insults. In this study, we investigated whether ASTX can inhibit alcohol-induced inflammation and oxidative stress in macrophages with the elucidation of mechanisms.
METHODS: RAW 264.7 macrophages and mouse bone marrow-derived macrophages (BMDM) were treated with 80 mM ethanol in the presence or absence of 25μM of ASTX for 72 h. Subsequently, the expression of genes related to inflammation and oxidative stress, cellular reactive oxygen species (ROS) accumulation, cellular NADlevel, and SIRT1 activity were measured. In addition, RAW 264.7 macrophages were treated with sirtinol or resveratrol, which are known inhibitor or activator of SIRT1 activity, respectively, to determine the contribution of SIRT1 to the inhibitory effect of ASTX on inflammation and oxidative stress in macrophages exposed to ethanol.
RESULTS: Ethanol increased mRNA expression of interleukin (Il)-6, Il-1b, and tumor necrosis factorα with a concomitant increase in nuclear translocation of nuclear factor κB, which was abolished by ASTX. Importantly, ethanol significantly decreased SIRT1 activity and cellular NADlevel, but ASTX markedly attenuated the decreases in RAW 264.7 macrophages. Sirtinol increased the expression of pro-inflammatory genes in ethanol-induced RAW 264.7 macrophages. In contrast, resveratrol decreased pro-inflammatory gene expression.
CONCLUSIONS: ASTX showed anti-inflammatory and antioxidant properties by inhibiting decreases in SIRT1 expression and cellular NADlevel in ethanol-treated macrophages. Therefore, ASTX may be used for the prevention of alcohol-induced cell damages.


greenmedinfo--2020-08-28--Astaxanthin-shifted gut microbiota is associated with inflammation and metabolic homeostasis.

BACKGROUND : Astaxanthin is a red lipophilic carotenoid that is often undetectable in human plasma due to the limited supply in typical Western diets .
Despite its presence at lower than detectable concentrations , previous clinical feeding studies have reported that astaxanthin exhibits potent antioxidant properties .
OBJECTIVE : We examined astaxanthin accumulation and its effects on gut microbiota , inflammation , and whole-body metabolic homeostasis in wild-type C57BL/6 J ( WT ) and β-carotene oxygenase 2 ( BCO2 ) knockout ( KO ) mice .
METHODS : Six-wk-old male and female BCO2 KO and WT mice were provided with @ @ @ @ @ @ @ diet ) or the control diet supplemented with 0.04 % astaxanthin ( wt/wt ) ad libitum for 8 wk .
Whole-body energy expenditure was measured by indirect calorimetry .
Feces were collected from individual mice for short-chain fatty acid assessment .
Hepatic astaxanthin concentrations and liver metabolic markers , cecal gut microbiota profiling , inflammation markers in colonic lamina propria , and plasma samples were assessed .
Data were analyzed by 3-way ANOVA followed by Tukey 's post hoc analysis .
RESULTS : BCO2 KO but not WT mice fed astaxanthin had∼10-fold more @ @ @ @ @ @ @ ( P CONCLUSIONS : Astaxanthin affects the gut microbiota composition in both genders , but the association with reductions in local and systemic inflammation , oxidative stress , and improvement of metabolic homeostasis only occurs in male mice .

BACKGROUND: Astaxanthin is a red lipophilic carotenoid that is often undetectable in human plasma due to the limited supply in typical Western diets. Despite its presence at lower than detectable concentrations, previous clinical feeding studies have reported that astaxanthin exhibits potent antioxidant properties.
OBJECTIVE: We examined astaxanthin accumulation and its effects on gut microbiota, inflammation, and whole-body metabolic homeostasis in wild-type C57BL/6 J (WT) and β-carotene oxygenase 2 (BCO2) knockout (KO) mice.
METHODS: Six-wk-old male and female BCO2 KO and WT mice were provided with either nonpurified AIN93M (e.g., control diet) or the control diet supplemented with 0.04% astaxanthin (wt/wt) ad libitum for 8 wk. Whole-body energy expenditure was measured by indirect calorimetry. Feces were collected from individual mice for short-chain fatty acid assessment. Hepatic astaxanthin concentrations and liver metabolic markers, cecal gut microbiota profiling, inflammation markers in colonic lamina propria, and plasma samples were assessed. Data were analyzed by 3-way ANOVA followed by Tukey's post hoc analysis.
RESULTS: BCO2 KO but not WT mice fed astaxanthin had∼10-fold more of this compound in liver than controls (P< 0.05). In terms of the microbiota composition, deletion of BCO2 was associated with a significantly increased abundance of Mucispirillum schaedleri in mice regardless of gender. In addition to more liver astaxanthin in male KO compared with WT mice fed astaxanthin, the abundance of gut Akkermansiamuciniphila was 385% greater, plasma glucagon-like peptide 1 was 27% greater, plasma glucagon and IL-1β were 53% and 30% lower, respectively, and colon NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation was 23% lower (all P< 0.05) in male KO mice than the WT mice.
CONCLUSIONS: Astaxanthin affects the gut microbiota composition in both genders, but the association with reductions in local and systemic inflammation, oxidative stress, and improvement of metabolic homeostasis only occurs in male mice.


greenmedinfo--2020-08-28--Astaxanthin attenuates pulmonary fibrosis through lncITPF and mitochondria‐mediated signal pathways.

Pulmonary fibrosis is a chronic interstitial lung disease characterized by pulmonary epithelial injury , fibroblast activation , extracellular matrix deposition , and tissue structure destruction .
However , an effective drug treatment remains unavailable .
Therefore , studying the mechanism of pulmonary fibrogenesis and finding effective drugs have become important problems in the field of respiratory diseases .
Pulmonary fibrosis is typically characterized by activated fibroblast proliferation and migration .
Hence , abnormality in activated fibroblast proliferation and migration is a major concern for treating pulmonary fibrosis .
Long noncoding RNA ( lncRNA ) is an enigmatic subclass of ncRNA @ @ @ @ @ @ @ participates in disease occurrence and development .
However , studies on lncRNA as the therapeutic target of drug action are rarely reported .
Our group first identified differentially expressed lncRNAs and revealed that lncITPF is a highly upregulated lncRNA in lung fibrosis .
In particular , lncITPF is detected in the blood of patients with idiopathic pulmonary fibrosis .
Clinical analysis shows that lncITPF is positively correlated with the degree of fibrosis .
The receiver operating characteristic ( ROC ) curve indicates that the specificity and sensitivity values are 95.0 and 64.3 , @ @ @ @ @ @ @ curve is 0.804 , indicating that lncITPF can be a diagnostic biomarker for IPF .
However , whether lncITPF is effective as a therapeutic target of drug action against pulmonary fibrosis remains unclear .
In this study , lncITPF acting as the therapeutic target of astaxanthin was explored in depth .
The findings elucidated that astaxanthin blocks the activated fibroblast proliferation and migration through lncITPF and mitochondria-mediated signal pathways to alleviate pulmonary fibrogenesis .

Pulmonary fibrosis is a chronic interstitial lung disease characterized by pulmonary epithelial injury, fibroblast activation, extracellular matrix deposition, and tissue structure destruction. However, an effective drug treatment remains unavailable. Therefore, studying the mechanism of pulmonary fibrogenesis and finding effective drugs have become important problems in the field of respiratory diseases. Pulmonary fibrosis is typically characterized by activated fibroblast proliferation and migration. Hence, abnormality in activated fibroblast proliferation and migration is a major concern for treating pulmonary fibrosis. Long noncoding RNA (lncRNA) is an enigmatic subclass of ncRNA that regulates various fundamental biological processes and participates in disease occurrence and development. However, studies on lncRNA as the therapeutic target of drug action are rarely reported. Our group first identified differentially expressed lncRNAs and revealed that lncITPF is a highly upregulated lncRNA in lung fibrosis. In particular, lncITPF is detected in the blood of patients with idiopathic pulmonary fibrosis. Clinical analysis shows that lncITPF is positively correlated with the degree of fibrosis. The receiver operating characteristic (ROC) curve indicates that the specificity and sensitivity values are 95.0 and 64.3, respectively. The area under the ROC curve is 0.804, indicating that lncITPF can be a diagnostic biomarker for IPF. However, whether lncITPF is effective as a therapeutic target of drug action against pulmonary fibrosis remains unclear. In this study, lncITPF acting as the therapeutic target of astaxanthin was explored in depth. The findings elucidated that astaxanthin blocks the activated fibroblast proliferation and migration through lncITPF and mitochondria-mediated signal pathways to alleviate pulmonary fibrogenesis.


greenmedinfo--2020-08-28--Purified astaxanthin from Haematococcus pluvialis promotes tissue regeneration.

Intracellular reactive apoptosis and reactive oxygen species ( ROS ) play a crucial role in ultraviolet- ( UV- ) induced inflammation and aging reaction in human dermal tissues .
This study determines the mechanism by whichextracts ( HPE ) and purified astaxanthin ( HPA ) to promote skin regeneration in the injured tissueand .
The results show that HPE and HPA decrease the DNA damage and promote the secretion of collagen from the human normal fibroblast cell line ( Hs68 ) in a dose-dependent manner .
UV irradiation and HPA reduce oxidative stress damage due to phorbol-12-myristate-13-acetate ( PMA ) @ @ @ @ @ @ @ free radicals , cells undergo a programmed cellular death .
Cellular apoptotic death is determined using annexin V-fluorescein isothiocyanate ( FITC ) /propidium iodide ( PI ) double staining to verify that there is no cell membrane asymmetry and that the nuclear membrane is broken .
Inflammatory symptoms and apoptotic injuries to experimental rats in a group that is treated with HPA treated are decreased in a dose-dependent manner after UVB exposure ( 300 mJ/cm ) for 15 min , compared to the vehicle control group .
These positive results show that HPA @ @ @ @ @ @ @ by conducting electrons out of cells to maintain a low level of oxidative stress so that collagen is synthesizedand .

Intracellular reactive apoptosis and reactive oxygen species (ROS) play a crucial role in ultraviolet- (UV-) induced inflammation and aging reaction in human dermal tissues. This study determines the mechanism by whichextracts (HPE) and purified astaxanthin (HPA) to promote skin regeneration in the injured tissueand. The results show that HPE and HPA decrease the DNA damage and promote the secretion of collagen from the human normal fibroblast cell line (Hs68) in a dose-dependent manner. UV irradiation and HPA reduce oxidative stress damage due to phorbol-12-myristate-13-acetate (PMA). When skin cells are injured by free radicals, cells undergo a programmed cellular death. Cellular apoptotic death is determined using annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining to verify that there is no cell membrane asymmetry and that the nuclear membrane is broken. Inflammatory symptoms and apoptotic injuries to experimental rats in a group that is treated with HPA treated are decreased in a dose-dependent manner after UVB exposure (300 mJ/cm) for 15 min, compared to the vehicle control group. These positive results show that HPA repairs UVB-triggered skin tissue injury and aging by conducting electrons out of cells to maintain a low level of oxidative stress so that collagen is synthesizedand.


greenmedinfo--2020-08-28--These findings suggest that astragaloside IV is a multifaceted renoprotective candidate drug for dia

These findings suggest that astragaloside IV is a multifaceted renoprotective candidate drug for diabetic nephropathy.

Astragaloside IV ( AS-IV ) has a variety of biological activities and is widely used to treat kidney diseases .
We conducted a systematic review of 24 animal studies including 424 animals to evaluate the efficacy of AS-IV for diabetic nephropathy ( DN ) ; all current possible mechanisms were summarized .
A search strategy was applied to eight databases from inception to June 2020 .
The CAMARADES 10-item quality checklist and Rev-Man 5.3 software were used to analyze the risks of bias of each study and data regarding outcome measures , respectively .
The mean study quality score was @ @ @ @ @ @ @ .
Meta-analyses data and comparisons between groups showed that AS-IV significantly slowed the progression of pathological signs in the kidney including glomeruli and tubules , increasing creatinine clearance rate , decreasing blood urea nitrogen , serum creatinine , 24-h urinary neutrophil gelatinase-associated lipocalin and N-acetyl -- D-glucosaminidase , 24-h urinary albumin , 24-h urinary microalbumin and HbA1c .
There were no significant differences between experimental and control groups with respect to mortality or levels of alanine aminotransferase and aspartate aminotransferase .
In terms of the possible mechanisms of treatment of DN , AS-IV @ @ @ @ @ @ @ antiapoptotic mechanisms , thereby alleviating endoplasmic reticulum stress , inhibiting mitochondrial fission , and increasing autophagic activity .
Taken together , our findings suggest that AS-IV is a multifaceted renoprotective candidate drug for DN .

Astragaloside IV (AS-IV) has a variety of biological activities and is widely used to treat kidney diseases. We conducted a systematic review of 24 animal studies including 424 animals to evaluate the efficacy of AS-IV for diabetic nephropathy (DN); all current possible mechanisms were summarized. A search strategy was applied to eight databases from inception to June 2020. The CAMARADES 10-item quality checklist and Rev-Man 5.3 software were used to analyze the risks of bias of each study and data regarding outcome measures, respectively. The mean study quality score was 5.4 points (range 3-8 points). Meta-analyses data and comparisons between groups showed that AS-IV significantly slowed the progression of pathological signs in the kidney including glomeruli and tubules, increasing creatinine clearance rate, decreasing blood urea nitrogen, serum creatinine, 24-h urinary neutrophil gelatinase-associated lipocalin and N-acetyl--D-glucosaminidase, 24-h urinary albumin, 24-h urinary microalbumin and HbA1c. There were no significant differences between experimental and control groups with respect to mortality or levels of alanine aminotransferase and aspartate aminotransferase. In terms of the possible mechanisms of treatment of DN, AS-IV acts through antifibrotic, antioxidant, and antiapoptotic mechanisms, thereby alleviating endoplasmic reticulum stress, inhibiting mitochondrial fission, and increasing autophagic activity. Taken together, our findings suggest that AS-IV is a multifaceted renoprotective candidate drug for DN.


greenmedinfo--2020-08-28--Astragaloside IV prevents Aβ 1-42 oligomers-induced memory impairment and hippocampal cell apoptosis

Astragaloside IV prevents Aβ 1-42 oligomers-induced memory impairment and hippocampal cell apoptosis.

Astragaloside IV ( AS-IV ) , a natural product derived from Radix Astragali ( Astragalus membranaceus ) , is beneficial for the treatment of Alzheimer 's disease ( AD ) , but the mechanisms underlying this benefit are not completely understood .
Peroxisome proliferator-activated receptor gamma ( PPARγ ) and brain-derived neurotrophic factor ( BDNF ) are potential therapeutic targets for AD .
In this study , we found that amyloid β protein fragment 1-42 oligomers ( AβO ) suppressed BDNF and PPARγ expression , and inhibited tyrosine receptor kinase B ( TrkB ) phosphorylation in cultured hippocampal neurons ; @ @ @ @ @ @ @ AS-IV .
Inhibition of PPARγ by genetic and pharmacological methods also blocked the effect of AS-IV on BDNF expression in AβO-treated cells .
Importantly , exogenous BDNF protected against neurotoxicity and apoptosis induced by AβO , whereas inhibition of PPARγ reversed protective effects of AS-IV against these outcomes .
In vivo data further revealed that AS-IV improved AβO-induced memory impairment and reduced apoptosis of hippocampal neurons .
Moreover , AS-IV suppressed the AβO-induced reduction in BDNF by promoting PPARγ activation inthe hippocampus .
Taken together , these results indicate that AS-IV prevents AβO-induced @ @ @ @ @ @ @ probably by promoting the PPARγ/BDNF signaling pathway .

Astragaloside IV (AS-IV), a natural product derived from Radix Astragali (Astragalus membranaceus), is beneficial for the treatment of Alzheimer's disease (AD), but the mechanisms underlying this benefit are not completely understood. Peroxisome proliferator-activated receptor gamma (PPARγ) and brain-derived neurotrophic factor (BDNF) are potential therapeutic targets for AD. In this study, we found that amyloid β protein fragment 1-42 oligomers (AβO) suppressed BDNF and PPARγ expression, and inhibited tyrosine receptor kinase B (TrkB) phosphorylation in cultured hippocampal neurons; these changes were ameliorated by treatment with AS-IV. Inhibition of PPARγ by genetic and pharmacological methods also blocked the effect of AS-IV on BDNF expression in AβO-treated cells. Importantly, exogenous BDNF protected against neurotoxicity and apoptosis induced by AβO, whereas inhibition of PPARγ reversed protective effects of AS-IV against these outcomes. In vivo data further revealed that AS-IV improved AβO-induced memory impairment and reduced apoptosis of hippocampal neurons. Moreover, AS-IV suppressed the AβO-induced reduction in BDNF by promoting PPARγ activation inthe hippocampus. Taken together, these results indicate that AS-IV prevents AβO-induced memory impairment and hippocampal neuronal apoptosis, probably by promoting the PPARγ/BDNF signaling pathway.


greenmedinfo--2020-08-28--These data indicate that astragaloside IV prevents aging via mainly improving age-related functional

These data indicate that astragaloside IV prevents aging via mainly improving age-related functional declines.

Astragaloside IV ( AS-IV ) is a representative component of astragaloside saponins in dried roots of Astragali Radix .
Astragaloside possesses a broad spectrum of pharmacological activities , including antibacterial , anti-fibrosis , anti-oxidant , anti-inflammatory and neuroprotective effects .
However , the role of AS-IV on anti-aging remains unclear .
In this paper , we studied the function of AS-IV on anti-aging using Caenorhabditis elegans ( C. elegans ) model .
We showed that AS-IV can prolong the lifespan of C. elegans in a natural aging model , a paraquat injury model and a heat stress model and improve @ @ @ @ @ @ @ indicate an improvement of glutamate content and decrease in glucose in the AS-IV treatment group compared to the control .
Further investigation revealed that AS-IV can induce the mRNA expressions of superoxide dismutase ( SOD ) and catalase ( CAT ) genes and increase the activities of SOD and CAT in the nematode .
Interestingly , AS-IV could not extend the lifespan of sod-1 , sod-2 , sod-3 , sod-4 , sod-5 , ctl-1 , ctl-2 , ctl-3 and daf-16 mutants .
These data indicate that AS-IV prevents aging via mainly improving age-related @ @ @ @ @ @ @ nematodes and partially modulating the IIS pathway activity .
Our results provide new insights into how AS-IV prevents and treats aging .

Astragaloside IV (AS-IV) is a representative component of astragaloside saponins in dried roots of Astragali Radix. Astragaloside possesses a broad spectrum of pharmacological activities, including antibacterial, anti-fibrosis, anti-oxidant, anti-inflammatory and neuroprotective effects. However, the role of AS-IV on anti-aging remains unclear. In this paper, we studied the function of AS-IV on anti-aging using Caenorhabditis elegans (C. elegans) model. We showed that AS-IV can prolong the lifespan of C. elegans in a natural aging model, a paraquat injury model and a heat stress model and improve movement capacity of nematodes. 1H-NMR data indicate an improvement of glutamate content and decrease in glucose in the AS-IV treatment group compared to the control. Further investigation revealed that AS-IV can induce the mRNA expressions of superoxide dismutase (SOD) and catalase (CAT) genes and increase the activities of SOD and CAT in the nematode. Interestingly, AS-IV could not extend the lifespan of sod-1, sod-2, sod-3, sod-4, sod-5, ctl-1, ctl-2, ctl-3 and daf-16 mutants. These data indicate that AS-IV prevents aging via mainly improving age-related functional declines, the antioxidant capacity of nematodes and partially modulating the IIS pathway activity. Our results provide new insights into how AS-IV prevents and treats aging.