greenmedinfo--2020-05-14--Carvacrol reduces hippocampal cell death and improves learning and memory deficits following lead-in

Carvacrol reduces hippocampal cell death and improves learning and memory deficits following lead-induced neurotoxicity via antioxidant activity.

Carvacrol is a monoterpene with neuroprotective effects in several animal models of neurodegeneration , including epilepsy , ischemia , and traumatic neuronal events .
In this study , we aimed to examine the effects of carvacrol on neurodegeneration induced by lead acetate in rats .
A total of 50 male Wistar rats were divided into five equal groups .
The control group received drinking water , while the neurotoxic group was exposed to 500 ppm of lead acetate in drinking water for 40 days .
The three remaining groups , which were also exposed to 500 ppm of lead acetate @ @ @ @ @ @ @ , 50 , and 100 mg/kg orally for 40 days .
The Morris water maze test was employed to examine spatial learning and memory .
Pathological damage to the hippocampus was determined by Nissl staining .
The level of malondialdehyde ( MDA ) , superoxide dismutase ( SOD ) , and catalase ( CAT ) were detected using biochemical analysis and the free radical scavenging activity as evaluated by the DPPH test .
Administration of carvacrol significantlyrestored learning and memory impairment induced by lead acetate .
Moreover , carvacrol ameliorated neurodegeneration , antioxidative @ @ @ @ @ @ @ hippocampus of rats exposed to lead .
The present results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity .

Carvacrol is a monoterpene with neuroprotective effects in several animal models of neurodegeneration, including epilepsy, ischemia, and traumatic neuronal events. In this study, we aimed to examine the effects of carvacrol on neurodegeneration induced by lead acetate in rats. A total of 50 male Wistar rats were divided into five equal groups. The control group received drinking water, while the neurotoxic group was exposed to 500 ppm of lead acetate in drinking water for 40 days. The three remaining groups, which were also exposed to 500 ppm of lead acetate, received carvacrol at doses of 25, 50, and 100 mg/kg orally for 40 days. The Morris water maze test was employed to examine spatial learning and memory. Pathological damage to the hippocampus was determined by Nissl staining. The level of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were detected using biochemical analysis and the free radical scavenging activity as evaluated by the DPPH test. Administration of carvacrol significantlyrestored learning and memory impairment induced by lead acetate. Moreover, carvacrol ameliorated neurodegeneration, antioxidative capacity, and lipid peroxidation in the hippocampus of rats exposed to lead. The present results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity.


greenmedinfo--2020-05-14--This study provided the evidence regarding the protective effects of carvacrol and thymol against Aβ

Background : Our previous findings indicated that carvacrol and thymol alleviate cognitive impairments caused by Aβ in rodent models of Alzheimer 's disease ( AD ) .
In this study , the neuroprotective effects of carvacrol and thymol against Aβ25-35-induced cytotoxicity were evaluated , and the potential mechanisms were determined .
Methods : PC12 cells were pretreated with Aβ25-35 for 2 h , followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by the 3- ( 4,5-dimethylthiazol-2-yl ) -2,5-diphenyltetrazolium bromide method .
A flurospectrophotometer was employed to observe the intracellular reactive oxygen species ( @ @ @ @ @ @ @ ( PKC ) activity was analyzed using ELISA .
Results : Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Aβ25-35-induced cytotoxicity .
Furthermore , Aβ25-35 could induce intracellular ROS production , while carvacrol and thymol could reverse this effect .
Moreover , our findings showed that carvacrol and thymol elevate PKC activity similar to Bryostatin-1 , as a PKC activator .
Conclusion : This study provided the evidence regarding the protective effects of carvacrol and thymol against Aβ25–35-induced cytotoxicity in PC12 cells .
The results suggested that the @ @ @ @ @ @ @ might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein .
Thus , carvacrol and thymol were found to have therapeutic potential in preventing or modulating AD .

Background: Our previous findings indicated that carvacrol and thymol alleviate cognitive impairments caused by Aβ in rodent models of Alzheimer's disease (AD). In this study, the neuroprotective effects of carvacrol and thymol against Aβ25-35-induced cytotoxicity were evaluated, and the potential mechanisms were determined.
Methods: PC12 cells were pretreated with Aβ25-35 for 2 h, followed by incubation with carvacrol or thymol for additional 48 h. Cell viability was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. A flurospectrophotometer was employed to observe the intracellular reactive oxygen species (ROS) production. Protein kinase C (PKC) activity was analyzed using ELISA.
Results: Our results indicated that carvacrol and thymol could significantly protect PC12 cells against Aβ25-35-induced cytotoxicity. Furthermore, Aβ25-35 could induce intracellular ROS production, while carvacrol and thymol could reverse this effect. Moreover, our findings showed that carvacrol and thymol elevate PKC activity similar to Bryostatin-1, as a PKC activator.
Conclusion: This study provided the evidence regarding the protective effects of carvacrol and thymol against Aβ25–35-induced cytotoxicity in PC12 cells. The results suggested that the neuroprotective effects of these compounds against Aβ25-35 might be through attenuating oxidative damage and increasing the activity of PKC as a memory-related protein. Thus, carvacrol and thymol were found to have therapeutic potential in preventing or modulating AD.


greenmedinfo--2020-05-14--Evaluation of the antibacterial activity and efflux pump reversal of thymol and carvacrol against St

Evaluation of the antibacterial activity and efflux pump reversal of thymol and carvacrol against Staphylococcus aureus.

The antibacterial activity and efflux pump reversal of thymol and carvacrol were investigated against theIS-58 strain in this study , @ @ @ @ @ against .
The minimum inhibitory concentration ( MIC ) was determined using the broth microdilution @ @ @ @ @ inhibition was assessed by reduction of the antibiotic and ethidium bromide ( EtBr ) MICs.toxicity @ @ @ @ @ method .
Both thymol and carvacrol presented antibacterial activities with MICs of 72 and 256µg/mL @ @ @ @ @ between thymol and tetracycline demonstrated synergism , while the association between carvacrol and tetracycline presented @ @ @ @ @ EtBr combinations did not differ from controls .
Thymol and carvacrol toxicity againstwere evidenced with @ @ @ @ @ , respectively , with 48 h of exposure .
In conclusion , the compounds presented @ @ @ @ @ tested strain , although no efficacy was observed in terms of efflux pump inhibition .

The antibacterial activity and efflux pump reversal of thymol and carvacrol were investigated against theIS-58 strain in this study, as well as their toxicity against. The minimum inhibitory concentration (MIC) was determined using the broth microdilution method, while efflux pump inhibition was assessed by reduction of the antibiotic and ethidium bromide (EtBr) MICs.toxicity was tested using the fumigation method. Both thymol and carvacrol presented antibacterial activities with MICs of 72 and 256µg/mL, respectively. The association between thymol and tetracycline demonstrated synergism, while the association between carvacrol and tetracycline presented antagonism. The compound and EtBr combinations did not differ from controls. Thymol and carvacrol toxicity againstwere evidenced with ECvalues of 17.96 and 16.97µg/mL, respectively, with 48 h of exposure. In conclusion, the compounds presented promising antibacterial activity against the tested strain, although no efficacy was observed in terms of efflux pump inhibition.


greenmedinfo--2020-05-14--Carvacrol exerted an anti-hyperglycemic effect in streptozotocin-induced diabetes.

BACKGROUND : Carvacrol is a food additive with various bioactivities , including reducing the blood glucose level as well as improvement of heart function , in diabetic mice .
We explored the antihyperglycemic effect of carvacrol and its effect on the key hepatic enzymes accounting for glucose metabolism .
METHODS : A streptozotocin ( STZ ) -induced diabetes-mellitus model in mice was used .
Mice were divided randomly into a control group , diabetic group , low dose carvacrol-treated diabetic group ( 10 mg/kg body weight [ BW ] ) , and high dose carvacrol-treated diabetic group ( 20 mg/kg @ @ @ @ @ @ @ ( i.p . )
in each carvacrol-treated group daily for 4 weeks and 6 weeks , respectively .
The level of random plasma glucose , fasting plasma glucose , and plasma insulinwas determined at 4 weeks and 6 weeks after carvacrol administration .
The plasma level of total cholesterol ( TC ) , triglycerides ( TG ) , aspartate aminotransferase ( AST ) , alanine aminotransferase ( ALT ) , alkaline phosphatase ( ALP ) , lactate dehydrogenase ( LDH ) , and the activity of hepatic key enzymesrelated to glucose metabolism were @ @ @ @ @ @ @ the levels of random plasma glucose and fasting plasma glucose , significantly in a dose-dependent manner .
A significant improvement in glucose tolerance and a significant decrease in the plasma level of TG were observed in carvacrol-treated diabetic mice at a dose of 20 mg/kg BW compared with that in vehicle-treated diabetic mice .
There was no significant difference in the plasma level of TC and insulin between vehicle-treated diabetic mice and carvacrol-treated diabetic mice .
Carvacrol treatment at a dose of 20 mg/kg BW significantly reduced the plasma levelof LDH but not @ @ @ @ @ @ @ compared with that in the vehicle-treated diabetic group .
The activity of hexokinase ( HK ) , 6-phosphofructokinase ( PFK ) , and citrate synthetase ( CS ) was increased by carvacrol treatment in diabetic mice .
CONCLUSIONS : Carvacrol exerted an anti-hyperglycemic effect in STZ-induced diabetic mice .
This was achieved through regulating glucose metabolism by increasing the activity of the hepatic enzymes HK , PFK , and CS .

BACKGROUND: Carvacrol is a food additive with various bioactivities, including reducing the blood glucose level as well as improvement of heart function, in diabetic mice. We explored the antihyperglycemic effect of carvacrol and its effect on the key hepatic enzymes accounting for glucose metabolism.
METHODS: A streptozotocin (STZ)-induced diabetes-mellitus model in mice was used. Mice were divided randomly into a control group, diabetic group, low dose carvacrol-treated diabetic group (10 mg/kg body weight [BW]), and high dose carvacrol-treated diabetic group (20 mg/kg BW). Carvacrol was injected intraperitoneally (i.p.) in each carvacrol-treated group daily for 4 weeks and 6 weeks, respectively. The level of random plasma glucose, fasting plasma glucose, and plasma insulinwas determined at 4 weeks and 6 weeks after carvacrol administration. The plasma level of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and the activity of hepatic key enzymesrelated to glucose metabolism were determined.
RESULTS: Carvacrol treatment decreased the levels of random plasma glucose and fasting plasma glucose, significantly in a dose-dependent manner. A significant improvement in glucose tolerance and a significant decrease in the plasma level of TG were observed in carvacrol-treated diabetic mice at a dose of 20 mg/kg BW compared with that in vehicle-treated diabetic mice. There was no significant difference in the plasma level of TC and insulin between vehicle-treated diabetic mice and carvacrol-treated diabetic mice. Carvacrol treatment at a dose of 20 mg/kg BW significantly reduced the plasma levelof LDH but not AST, ALT, or ALP, compared with that in the vehicle-treated diabetic group. The activity of hexokinase (HK), 6-phosphofructokinase (PFK), and citrate synthetase (CS) was increased by carvacrol treatment in diabetic mice.
CONCLUSIONS: Carvacrol exerted an anti-hyperglycemic effect in STZ-induced diabetic mice. This was achieved through regulating glucose metabolism by increasing the activity of the hepatic enzymes HK, PFK, and CS.


greenmedinfo--2020-05-14--Natural compounds rosmarinic acid and carvacrol counteract aluminium-induced oxidative stress.

Aluminum accumulation , glutathione ( GSH ) and malondialdehyde ( MDA ) concentrations as well as catalase ( CAT ) and superoxide dismutase ( SOD ) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al ( 7.5 mg/kg/day ( 0.15 LD ) as AlCl ( 37.08 mg/kg/day ) , whereas HCl ( 30.41 mg/kg/day ) was used as Clcontrol , the treatments were performed for 21 days , i.p.
, in the presence and absence of rosmarinic acid ( 0.2805 mg/kg/day ( 0.05 LD ) , 21 days , i.g . )
or @ @ @ @ @ @ @ ) , 21 days , i.g. )
.
The treatment with AlClincreased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates .
Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates .
However , AlCltreatment led to Al accumulation in mice blood , brain , and liver and induced oxidative stress , assessed based on MDA concentration in the brain and liver .
Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing @ @ @ @ @ @ @ peroxidation .
AlCltreatment increased CAT activity in mice brain and liver homogenates , whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlClhad no significant effect on CAT activity .
SOD activity remained unchanged after all the treatments in our study .
We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation .

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al(7.5 mg/kg/day (0.15 LD) as AlCl(37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Clcontrol, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD), 21 days, i.g.). The treatment with AlClincreased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCltreatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCltreatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlClhad no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.


greenmedinfo--2020-05-14--Lemon balm and rosmarinic acid could improve liver damage by non-alcoholic lipid accumulation and ma

Lemon balm and rosmarinic acid could improve liver damage by non-alcoholic lipid accumulation and may be promising medications to treat NASH.

Nonalcoholic fatty liver disease ( NAFLD ) ranges in severity from hepatic steatosis to cirrhosis .
Lemon balm and its @ @ @ @ @ ( RA ) , effectively improve the liver injury and obesity ; however , their @ @ @ @ @ ( NASH ) are unknown .
In this study , we investigated the effects of @ @ @ @ @ extract ( LBE ) on NAFLD and liver fibrosis and elucidated their mechanisms .
Palmitic @ @ @ @ @ HepG2 cells and db/db mice fed a methionine- and choline-deficient ( MCD ) diet were @ @ @ @ @ human NASH .
LBE and RA treatments alleviated the oxidative stress by increasing antioxidant enzymes @ @ @ @ @ expression by the activation of adenosine monophosphate-activated protein kinase ( AMPK ) in vitro and @ @ @ @ @ RA treatments inhibited the expression of genes involved in hepatic fibrosis and inflammation in vitro @ @ @ @ @ , LBE and RA could improve liver damage by non-alcoholic lipid accumulation and may be @ @ @ @ @ .

Nonalcoholic fatty liver disease (NAFLD) ranges in severity from hepatic steatosis to cirrhosis. Lemon balm and its major constituent, rosmarinic acid (RA), effectively improve the liver injury and obesity; however, their therapeutic effects on nonalcoholic steatohepatitis (NASH) are unknown. In this study, we investigated the effects of RA and a lemon balm extract (LBE) on NAFLD and liver fibrosis and elucidated their mechanisms. Palmitic acid (PA)-exposed HepG2 cells and db/db mice fed a methionine- and choline-deficient (MCD) diet were utilized to exhibit symptoms of human NASH. LBE and RA treatments alleviated the oxidative stress by increasing antioxidant enzymes and modulated lipid metabolism-related gene expression by the activation of adenosine monophosphate-activated protein kinase (AMPK) in vitro and in vivo. LBE and RA treatments inhibited the expression of genes involved in hepatic fibrosis and inflammation in vitro and in vivo. Together, LBE and RA could improve liver damage by non-alcoholic lipid accumulation and may be promising medications to treat NASH.


greenmedinfo--2020-05-14--Overweight Before Age 40 Increases Cancer Risk by 70%

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greenmedinfo--2020-05-14--Lemon balm extracts prevent breast cancer progression.

Breast cancer is the most frequently diagnosed malignant pathology , representing the primary cause of cancer death in women .
Natural products are an appealing strategy to limit the progression of the disease .
Targeting angiogenesis in breast cancer may positively impact on poor prognosis of breast cancer .
As source of natural compounds , we investigated the leaves ofL .
( MO ) , known as lemon balm , an aromatic plant that spontaneously grows in the South and Western areas of Romania , being traditionally recommended as anxiolytic , antispasmodic , or as digestive remedy .
Our aim @ @ @ @ @ @ @ the antiangiogenic and chemopreventive bioactivity of MO from Banat region , on breast cancer .
Two ethanolic extracts of MO ( MOE96 and MOE70 ) and one methanolic extract ( MOM80 ) were subjected to polyphenol and triterpene profiling by HPLC-MS , and the antioxidant capacity was evaluated .
The antiangiogenic potential was investigated using the chorioallantoic membrane assay ( CAM ) .
The MTT ( 3- ( 4,5-dimethylthiazol-2-yl ) -2-5-diphenyltetrazolium bromide ) assay was used to investigate the cytotoxic effects on MCF-7 and MDA-MB-231breast cancer cells , as well as on MCF-10A @ @ @ @ @ @ @ was performed by DAPI staining .
Rosmarinic acid ( RA ) and ursolic acid ( UA ) were revealed as dominant phytocompounds .
The highest concentration in phytochemicals were found in MOM80 ; MOE96 was more concentrated in UA , while MOE70 extracted more RA .
MOE96 inhibited cancer progression and angiogenesis in the in ovo CAM model using MDA-MB-231 cells , inhibiting breast cancer progression and angiogenesis for the MDA-MB-231 breast cancer cell line ; no secondary tumoral areas were registered , indicative for a preventive effect against breast tumor cell invasiveness @ @ @ @ @ @ @ also exhibited by MOE96 , in particular against the estrogen receptor positive MCF7 breast cancer cell line , with no cytotoxic effect on healthy cells .
The estrogen receptor positive MCF7 cell line proved to be more sensitive to the extract antiproliferative activity than the triple negative MDA-MB-231 breast cancer cell line .
Nevertheless , the chemopreventive potential of MOE96 extract is phenotype-dependent and is rather related to the apoptosis and antiangiogenic effects suggesting a multitargeted mechanism of action due to its multiple compound composition next to a concentration ratio of RA : @ @ @ @ @ @

Breast cancer is the most frequently diagnosed malignant pathology, representing the primary cause of cancer death in women. Natural products are an appealing strategy to limit the progression of the disease. Targeting angiogenesis in breast cancer may positively impact on poor prognosis of breast cancer. As source of natural compounds, we investigated the leaves ofL. (MO), known as lemon balm, an aromatic plant that spontaneously grows in the South and Western areas of Romania, being traditionally recommended as anxiolytic, antispasmodic, or as digestive remedy. Our aim was to investigate the phytochemical profiling and the antiangiogenic and chemopreventive bioactivity of MO from Banat region, on breast cancer. Two ethanolic extracts of MO (MOE96 and MOE70) and one methanolic extract (MOM80) were subjected to polyphenol and triterpene profiling by HPLC-MS, and the antioxidant capacity was evaluated. The antiangiogenic potential was investigated using the chorioallantoic membrane assay (CAM). The MTT(3-(4,5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide) assay was used to investigate the cytotoxic effects on MCF-7 and MDA-MB-231breast cancer cells, as well as on MCF-10A normal breast epithelial cells, while apoptosis was performed by DAPI staining. Rosmarinic acid (RA) and ursolic acid (UA) were revealed as dominant phytocompounds. The highest concentration in phytochemicals were found in MOM80; MOE96 was more concentrated in UA, while MOE70 extracted more RA. MOE96 inhibited cancer progression and angiogenesis in the in ovo CAM model using MDA-MB-231 cells, inhibiting breast cancer progression and angiogenesis for the MDA-MB-231 breast cancer cell line; no secondary tumoral areas were registered, indicative for a preventive effect against breast tumor cell invasiveness. The highest cell inhibitory activity was also exhibited by MOE96, in particular against the estrogen receptor positive MCF7 breast cancer cell line, with no cytotoxic effect on healthy cells. The estrogen receptor positive MCF7 cell line proved to be more sensitive to the extract antiproliferative activity than the triple negative MDA-MB-231 breast cancer cell line. Nevertheless, the chemopreventive potential of MOE96 extract is phenotype-dependent and is rather related to the apoptosis and antiangiogenic effects suggesting a multitargeted mechanism of action due to its multiple compound composition next to a concentration ratio of RA : UA in favor of UA.


greenmedinfo--2020-05-14--This evidence shows a promising therapeutic role for rosmarinic acid in inflammatory status.

Rosmarinic acid ( RA ) is a potential herbal medicine and has received considerable attention due to its strong antioxidant properties .
The aim of this study is to investigate the impact of RA on inflammation and oxidative stress induced by lipopolysaccharide ( LPS ) in peripheral blood mononuclear cells ( PBMCs ) .
PBMCs were pre-treated with various contents of RA ( 20 , 40 , 80 µM ) for 24 h , then , stimulated with LPS ( 10 ng/ml ) for more 6 h. ELISA and Real-time PCR were done to detect the levels of IL-6 , @ @ @ @ @ @ @ .
Western blot was done to investigate the phosphorylated amounts of P65-NF-κB and JNK .
Inflammatory cytokines and oxidant-antioxidant parameters were determined by colorimetric and ELISA methods .
The results indicated that LPS augmented the protein levels of IL-6 , TNF-α , and IL-1β cytokines as well as the mRNA levels of IL-6 , TNF-α , IL-1β , COX-2 , and IL-10 cytokines in in PBMCs .
However , pretreatment with RA could reduce theimpact of LPS on inflammatory markers .
In addition , RA inhibited P65-NF-κB and JNK phosphorylation .
LPS also @ @ @ @ @ @ @ total thiol , and total antioxidant capacity as well as an increment in malondialdehyde and nitric oxide metabolite contents that RA abrogated them.Collectively , our finding demonstrated that RA ameliorates LPS-induced inflammation in PBMCs .
RA reduces oxidative stress by preventing lipid peroxidation and nitric oxide production as well as restarting the activity of the GPx and SOD enzymes .
Furthermore , our findings indicated that RA was ableto protect PBMCs from inflammation via inhibiting the NF-κB and JNK MAPK pathways .
This evidence shows a promising therapeutic role for RA in inflammatory @ @

Rosmarinic acid (RA) is a potential herbal medicine and has received considerable attention due to its strong antioxidant properties. The aim of this study is to investigate the impact of RA on inflammation and oxidative stress induced by lipopolysaccharide (LPS) in peripheral blood mononuclear cells (PBMCs). PBMCs were pre-treated with various contents of RA (20, 40, 80 µM) for 24 h, then, stimulated with LPS (10 ng/ml) for more 6 h. ELISA and Real-time PCR were done to detect the levels of IL-6, TNF-α, COX-2, IL-1β and IL-10. Western blot was done to investigate the phosphorylated amounts of P65-NF-κB and JNK. Inflammatory cytokines and oxidant-antioxidant parameters were determined by colorimetric and ELISA methods. The results indicated that LPS augmented the protein levels of IL-6, TNF-α, and IL-1β cytokines as well as the mRNA levels of IL-6, TNF-α, IL-1β, COX-2, and IL-10 cytokines in in PBMCs. However, pretreatment with RA could reduce theimpact of LPS on inflammatory markers. In addition, RA inhibited P65-NF-κB and JNK phosphorylation. LPS also caused a decrease in antioxidant enzymes, total thiol, and total antioxidant capacity as well as an increment in malondialdehyde and nitric oxide metabolite contents that RA abrogated them.Collectively, our finding demonstrated that RA ameliorates LPS-induced inflammation in PBMCs. RA reduces oxidative stress by preventing lipid peroxidation and nitric oxide production as well as restarting the activity of the GPx and SOD enzymes. Furthermore, our findings indicated that RA was ableto protect PBMCs from inflammation via inhibiting the NF-κB and JNK MAPK pathways. This evidence shows a promising therapeutic role for RA in inflammatory status.


greenmedinfo--2020-05-14--New Bill (H.R.6666) Could Cement In Place the COVID-19 Medical Police State - Stand To Oppose Now

A new bill has been introduced into the 116th Congress ( 2019-2020 ) of the U.S. House of Representatives named H.R.6666 - COVID-19 Testing , Reaching , And Contacting Everyone ( TRACE ) Act , with the potential to further the loss of the already vanishing health freedoms of each and every citizen of the United States .
You can stand with us today by opposing H.R.6666 now ( use this link to Take A Stand ) H.R .
6666 , despite having been introduced by Rep. Bobby L. Rush [ D-IL-1 ] and referred to the Referred to the @ @ @ @ @ @ @ the same day almost two weeks ago on 5/01/2020 , has received little mainstream media coverage to this date , other than recent attempts to debunk claims that it would further violate the rights of Americans .
As of 5/14/2020 is has 59 co-sponsors , including one Republican , indicating the potential that it may gain greater bipartisan support unless strongly opposed .
H.R .
6666 authorizes the Secretary of Health and Human Services , acting through the Director of the CDC , to allocate a 100 billion dollars , annually ( or @ @ @ @ @ @ @ over ) , to employ , train , and deploy an immense workforce of “ testing and contact tracers ” to be sent directly to everyone ’ s homes for diagnostic testing and tracing of contacts suspected to have been infected or are at risk of infection with COVID-19 .
The bill uses broad yet highly vague language to describe the role of this veritable army of new agents of the emerging U.S. medical police state “ for other purposes , ” such as “ support the quarantine of such contacts.
” The @ @ @ @ @ @ @ the government and public and private grantees under its coordination unusually broad discretion to apply its newly granted police powers under the presently defined “ national COVID health emergency.
” Since the national lockdown began on March the 15th , we ’ ve witnessed the near complete suspension of most of our Constitutionally irrevocable civil liberties , with the near complete cessation and/or modification of all socio-economic activity within the country .
Moreover , executive orders have already been enacted throughout this country enabling the forced seizure of body tissue and fluids , @ @ @ @ @ @ @ isolation , quarantine and arrest without due process .
While not all of these draconian regulations have yet been implemented en masse , they exist in the letter of the law and therefore could be enforced , especially given that bills such as H.R.6666 use broad discretionary language leaving it to the government to intepret its meaning and apply force as it sees fit .
If H.R .
6666 passes , real `` teeth '' would be put to many of the laws , acts , orders , and regulations that have been @ @ @ @ @ @ @ two months , potentially locking the entire country into an irreversible control grid the likes of which we have not seen outside of countries like China .
In light of this , H.R .
6666 may be setting the stage for the implementation of what WHO director Dr. Mike Ryan of the WHO and Ventura County California officials , say will include forcibly removing family members found positive or suspected of being infected .
The only way to prevent this is to make sure the bill is opposed and dies .
Eligible recipients @ @ @ @ @ @ @ “ school-based ” institutions , implying that these organizations might also become , in part , testing or treatment centers .
Take a few minutes to watch the important reports by independent journalists Spyro Skouras and James Corbett on the contact tracing agenda in the rapidly unfolding story of coronavirus .
Contract tracing , which on the surface appears to mitigate the risk of disease spread by identifying carriers and interfering their further contact with the healthy , is based on a series of flawed assumptions : • The disease known as COVID-19 @ @ @ @ @ @ @ singular infectious disease entity , i.e .
the viral particle known as SARS-CoV-2 , has never been validated through Koch postulates to be inducible and solely caused by SARS-CoV-2 within a controlled clinical or experimental setting .
Over 100 different types of coronavirus have already been identified in circulation naturally around the world , and there is serious doubt that we can adequately distinguish between natural extracellular vesicles such as human exosomes and novel or endogenous forms of coronovirus already present in the human virome with the tests being used today , namely @ @ @ @ @ @ @ at www.questioningcovid.com • That so-called “ positive cases ” identified through any number of over 100 different PCR-based and antibody-testing methods are accurate indicators of the presence of COVID-19 , or do not generate false positives .
If false positives are not accounted for , contract tracing can cause or contribute to a falsely expanding epidemic and those who are unnecessarily quarantined and treated will succumb to greatly elevated iatrogenically induced morbidity and mortality risks , which will never be discovered because the so-called “ confirmed case fatality rates for COVID-19 ” require @ @ @ @ @ @ @ suspicion of infection.
” This is because the WHO and US Vital Statistics agencies explicitly advise against confirming these suspicion-based deaths through viral testing and other clinical means , in an egregious departure from both science and evidence-based medicine .
If contact tracing is fraught with technical inadequacies , why would it be so aggressively implemented nationwide ?
One reason is that it provides a justification for total spectrum dominance via real-time surveillance and control of the entire population under the auspices of “ public health safety , ” into perpetuity .
In @ @ @ @ @ @ @ “ war on terror , ” but with the enemy being defined as our own bodies , or contact between bodies , and the solution the complete removal of any privacy , nor right to exempt oneself or children from medical mandates .
The system would likely include tracking GPS data of mobile device users and then following back their contacts to identify , test , isolate , quarantine , medicate , or otherwise vaccinate them when one becomes available most likely in the fall of 2020 .
The media has already fomented @ @ @ @ @ @ @ and catastrophizing case fatality projections , over the past few months .
Their egregious disregard for the truth has lead to socioenomic and psychobiological impacts that are arguably orders of magnitude more harmful and deadly than this , or any other virus believed to contribute to flu-like illness .
Clearly , the media and power that be could re-manufacture another crisis , or “ second ” or “ third ” wave simply be repeating what they have already one ( learn more on the topic via the Corbett Report ) .
At which @ @ @ @ @ @ @ tracers , testers , quarantine enforcers , and medicators and vaccinators , the systems being funded by H.R .
6666 would be ready to further this agenda .
So , why does H.R .
6666 refrain from providing even the most rudimentary details to how one of the largest and most widespread in impact bills ever introduced will impact those affected ?
The more vague and broad the language , the less oversight .
The truth is that the detailed plans for how H.R.666 will be implemented were already written and revealed to @ @ @ @ @ @ @ Rockefeller Foundation in a 30-page plan titled , “ NATIONAL COVID-19 TESTING ACTION PLAN : Pragmatic steps to reopen our workplaces and our communities.
” Not coincidentally , the plan proposed the exact same dollar figure was required - 100 billion dollars -- and suggested that between 100-300,000 contract tracers would be needed .
Please take a strong action today by using the health freedom advocacy portal and campaign on Stand For Health Freedom , or use the widget below .

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A new bill has been introduced into the 116th Congress (2019-2020) of the U.S. House of Representatives named H.R.6666 - COVID-19 Testing, Reaching, And Contacting Everyone (TRACE) Act, with the potential to further the loss of the already vanishing health freedoms of each and every citizen of the United States. You can stand with us today by opposing H.R.6666 now (use this link to Take A Stand)
H.R. 6666, despite having been introduced by Rep. Bobby L. Rush [D-IL-1] and referred to the Referred to the House Committee on Energy and Commerce on the same day almost two weeks ago on 5/01/2020, has received little mainstream media coverage to this date, other than recent attempts to debunk claims that it would further violate the rights of Americans. As of 5/14/2020 is has 59 co-sponsors, including one Republican, indicating the potential that it may gain greater bipartisan support unless strongly opposed.
H.R. 6666 authorizes the Secretary of Health and Human Services, acting through the Director of the CDC, to allocate a 100 billion dollars, annually (or until the national COVID emergency is declared over), to employ, train, and deploy an immense workforce of “testing and contact tracers” to be sent directly to everyone’s homes for diagnostic testing and tracing of contacts suspected to have been infected or are at risk of infection with COVID-19. The bill uses broad yet highly vague language to describe the role of this veritable army of new agents of the emerging U.S. medical police state “for other purposes,” such as “support the quarantine of such contacts.”
The nebulous language of H.R. 6666 affords the government and public and private grantees under its coordination unusually broad discretion to apply its newly granted police powers under the presently defined “national COVID health emergency.” Since the national lockdown began on March the 15th, we’ve witnessed the near complete suspension of most of our Constitutionally irrevocable civil liberties, with the near complete cessation and/or modification of all socio-economic activity within the country. Moreover, executive orders have already been enacted throughout this country enabling the forced seizure of body tissue and fluids, property, forced vaccination, testing, isolation, quarantine and arrest without due process. While not all of these draconian regulations have yet been implemented en masse, they exist in the letter of the law and therefore could be enforced, especially given that bills such as H.R.6666 use broad discretionary language leaving it to the government to intepret its meaning and apply force as it sees fit. If H.R. 6666 passes, real "teeth" would be put to many of the laws, acts, orders, and regulations that have been passed as executive orders over the past two months, potentially locking the entire country into an irreversible control grid the likes of which we have not seen outside of countries like China.
In light of this, H.R. 6666 may be setting the stage for the implementation of what WHO director Dr. Mike Ryan of the WHO and Ventura County California officials, say will include forcibly removing family members found positive or suspected of being infected. The only way to prevent this is to make sure the bill is opposed and dies.
Eligible recipients of funds include “faith-based” and “school-based” institutions, implying that these organizations might also become, in part, testing or treatment centers.
What is Contract Tracing?
Take a few minutes to watch the important reports by independent journalists Spyro Skouras and James Corbett on the contact tracing agenda in the rapidly unfolding story of coronavirus.
Contract tracing, which on the surface appears to mitigate the risk of disease spread by identifying carriers and interfering their further contact with the healthy, is based on a series of flawed assumptions:
The disease known as COVID-19 and believed to be caused by a singular infectious disease entity, i.e. the viral particle known as SARS-CoV-2, has never been validated through Koch postulates to be inducible and solely caused by SARS-CoV-2 within a controlled clinical or experimental setting. Over 100 different types of coronavirus have already been identified in circulation naturally around the world, and there is serious doubt that we can adequately distinguish between natural extracellular vesicles such as human exosomes and novel or endogenous forms of coronovirus already present in the human virome with the tests being used today, namely, RT-PCR. Learn more about this at www.questioningcovid.com That so-called “positive cases” identified through any number of over 100 different PCR-based and antibody-testing methods are accurate indicators of the presence of COVID-19, or do not generate false positives. If false positives are not accounted for, contract tracing can cause or contribute to a falsely expanding epidemic and those who are unnecessarily quarantined and treated will succumb to greatly elevated iatrogenically induced morbidity and mortality risks, which will never be discovered because the so-called “confirmed case fatality rates for COVID-19” require no viral testing, and only “suspicion of infection.” This is because the WHO and US Vital Statistics agencies explicitly advise against confirming these suspicion-based deaths through viral testing and other clinical means, in an egregious departure from both science and evidence-based medicine.
If contact tracing is fraught with technical inadequacies, why would it be so aggressively implemented nationwide? One reason is that it provides a justification for total spectrum dominance via real-time surveillance and control of the entire population under the auspices of “public health safety,” into perpetuity. In essence, it is like a new “war on terror,” but with the enemy being defined as our own bodies, or contact between bodies, and the solution the complete removal of any privacy, nor right to exempt oneself or children from medical mandates. The system would likely include tracking GPS data of mobile device users and then following back their contacts to identify, test, isolate, quarantine, medicate, or otherwise vaccinate them when one becomes available most likely in the fall of 2020. The media has already fomented profound fear through misreporting, misrepresenting, and catastrophizing case fatality projections, over the past few months. Their egregious disregard for the truth has lead to socioenomic and psychobiological impacts that are arguably orders of magnitude more harmful and deadly than this, or any other virus believed to contribute to flu-like illness. Clearly, the media and power that be could re-manufacture another crisis, or “second” or “third” wave simply be repeating what they have already one (learn more on the topic via the Corbett Report). At which point, with an army of contact tracers, testers, quarantine enforcers, and medicators and vaccinators, the systems being funded by H.R. 6666 would be ready to further this agenda.
So, why does H.R. 6666 refrain from providing even the most rudimentary details to how one of the largest and most widespread in impact bills ever introduced will impact those affected? The more vague and broad the language, the less oversight. The truth is that the detailed plans for how H.R.666 will be implemented were already written and revealed to the public a month ago by the Rockefeller Foundation in a 30-page plan titled, “NATIONAL COVID-19 TESTING ACTION PLAN:Pragmatic steps to reopen our workplaces and our communities.” Not coincidentally, the plan proposed the exact same dollar figure was required - 100 billion dollars -- and suggested that between 100-300,000 contract tracers would be needed.
Please take a strong action today by using the health freedom advocacy portal and campaign on Stand For Health Freedom, or use the widget below.


greenmedinfo--2020-05-14--Anti-osteoporotic effects of Salvia miltiorrhiza Bunge EtOH extract both in ovariectomized and natur

Anti-osteoporotic effects of Salvia miltiorrhiza Bunge EtOH extract both in ovariectomized and naturally menopausal mouse models.

ETHNOPHARMACOLOGICAL RELEVANCE : Salvia miltiorrhiza is a traditional oriental medicine widely used for preventing and treating disorders of the liver , menstrual , and blood circulation systems .
Osteoporosis , loss of bone with age and/or estrogen deficiency , is an important causal factor of fracture .
S. miltiorrhiza extract has been used to alleviate dysmenorrhea and painful osteoarthritis .
AIM OF THE STUDY : This study was performed to investigate the anti-osteoporosis activity of the Salvia miltiorrhiza ethanol extract ( SME ) in osteoporosis-prone conditions : ovariectomized ( OVX ) and naturally menopaused ( NM ) ICR mice .
@ @ @ @ @ @ @ SME ( 50-200 mg/kg ) were evaluated based on bone mineral density using microCT analysis , biochemical parameters , and changes in the gene expressions involved in bone resorption .
RESULTS : SME ameliorated the loss of trabecular bone both in OVX and NM mice .
SME was effective in correcting aberrant levels of RANKL , osteocalcin , and BALP , which are critically involved in bone resorption .
In addition , SME suppressed the expression of TRAF6 and NFATc1 , which play a role in osteoclast differentiation .
CONCLUSIONS : SME suppressed @ @ @ @ @ @ @ bone resorption and osteoclast differentiation both in OVX and NM mice .
SME is likely to be developed as a therapeutic agent for osteoporosis .

ETHNOPHARMACOLOGICAL RELEVANCE: Salvia miltiorrhiza is a traditional oriental medicine widely used for preventing and treating disorders of the liver, menstrual, and blood circulation systems. Osteoporosis, loss of bone with age and/or estrogen deficiency, is an important causal factor of fracture. S. miltiorrhiza extract has been used to alleviate dysmenorrhea and painful osteoarthritis.
AIM OF THE STUDY: This study was performed to investigate the anti-osteoporosis activity of the Salvia miltiorrhiza ethanol extract (SME) in osteoporosis-prone conditions: ovariectomized (OVX) and naturally menopaused (NM) ICR mice.
MATERIALS AND METHODS: Anti-osteoporotic potentials of SME (50-200 mg/kg) were evaluated based on bone mineral density using microCT analysis, biochemical parameters, and changes in the gene expressions involved in bone resorption.
RESULTS: SME ameliorated the loss of trabecular bone both in OVX and NM mice. SME was effective in correcting aberrant levels of RANKL, osteocalcin, and BALP, which are critically involved in bone resorption. In addition, SME suppressed the expression of TRAF6 and NFATc1, which play a role in osteoclast differentiation.
CONCLUSIONS: SME suppressed the loss of trabecular bone via suppressing bone resorption and osteoclast differentiation both in OVX and NM mice. SME is likely to be developed as a therapeutic agent for osteoporosis.


greenmedinfo--2020-05-14--Anti-obesity effects of tanshinone I from Salvia miltiorrhiza.

Tanshinone I ( Tan I ) is a diterpenoid isolated fromBunge and exhibits antitumor effects in several cancers .
However , the anti-obesity properties of Tan I remain unexplored .
Here , we evaluated the anti-obesity effects of Tan I in high-fat-diet ( HFD ) -induced obese mice and investigated the underlying molecular mechanisms in 3T3-L1 cells .
HFD-induced obese mice were orally administrated Tan I for eight weeks , and body weight , weight gain , hematoxylin and eosin staining and serum biological parameters were examined .
The adipogenesis of 3T3-L1 preadipocytes was assessed using Oil Red O staining @ @ @ @ @ @ @ ) levels , and mitotic clonal expansion ( MCE ) and its related signal molecules were analyzed during early adipogenesis of 3T3-L1 cells .
The administration of Tan I significantly reduced body weight , weight gain , and white adipocyte size , and improved obesity-induced serum levels of glucose , free fatty acid , total TG , and total cholesterol in vivo in HFD-induced obese mice .
Furthermore , Tan I-administered mice demonstrated improvement of glucose metabolism and insulin sensitivity .
Treatment with Tan I inhibited the adipogenesis of 3T3-L1 preadipocytes in vitro @ @ @ @ @ @ @ an early phase of adipogenesis through the attenuation of MCE via cell cycle arrest at the G1/S phase transition .
Tan I inhibited the phosphorylation of p38 , extracellular signal-regulated kinase ( ERK ) , and Akt during the process of MCE , while it stimulated the phosphorylation of AMP-activated protein kinase .
Furthermore , Tan I repressed the expression of CCAAT-enhancer-binding proteinβ ( ) , histone H3K9 demethylase , and subsequently cell cycle genes .
Moreover , Tan I regulated the expression of early adipogenic transcription factors including GATAs and Kruppel-like factor @ @ @ @ @ @ @ Tan I prevents HFD-induced obesity via the inhibition of early adipogenesis , and thus improves glucose metabolism and insulin sensitivity .
This suggests that Tan I possesses therapeutic potential for the treatment of obesity and obesity-related diseases .

Tanshinone I (Tan I) is a diterpenoid isolated fromBunge and exhibits antitumor effects in several cancers. However, the anti-obesity properties of Tan I remain unexplored. Here, we evaluated the anti-obesity effects of Tan I in high-fat-diet (HFD)-induced obese mice and investigated the underlying molecular mechanisms in 3T3-L1 cells. HFD-induced obese mice were orally administrated Tan I for eight weeks, and body weight, weight gain, hematoxylin and eosin staining and serum biological parameters were examined. The adipogenesis of 3T3-L1 preadipocytes was assessed using Oil Red O staining and measurement of intracellular triglyceride (TG) levels, and mitotic clonal expansion (MCE) and its related signal molecules were analyzed during early adipogenesis of 3T3-L1 cells. The administration of Tan I significantly reduced body weight, weight gain, and white adipocyte size, and improved obesity-induced serum levels of glucose, free fatty acid, total TG, and total cholesterol in vivo in HFD-induced obese mice. Furthermore, Tan I-administered mice demonstrated improvement of glucose metabolism and insulin sensitivity. Treatment with Tan I inhibited the adipogenesis of 3T3-L1 preadipocytes in vitro, with this inhibition mainly occurring at an early phase of adipogenesis through the attenuation of MCE via cell cycle arrest at the G1/S phase transition. Tan I inhibited the phosphorylation of p38, extracellular signal-regulated kinase (ERK), and Akt during the process of MCE, while it stimulated the phosphorylation of AMP-activated protein kinase. Furthermore, Tan I repressed the expression of CCAAT-enhancer-binding proteinβ (), histone H3K9 demethylase, and subsequently cell cycle genes. Moreover, Tan I regulated the expression of early adipogenic transcription factors including GATAs and Kruppel-like factor family factors. These results indicate that Tan I prevents HFD-induced obesity via the inhibition of early adipogenesis, and thus improves glucose metabolism and insulin sensitivity. This suggests that Tan I possesses therapeutic potential for the treatment of obesity and obesity-related diseases.


greenmedinfo--2020-05-14--Rosmarinic acid exhibits broad anti-enterovirus A71 activity.

Enterovirus A71 ( EV-A71 ) , a positive-stranded RNA virus of the Picornaviridae family , may cause neurological complications or fatality in children .
We examined specific factors responsible for this virulence using a chemical genetics approach .
Known compounds from an anti-EV-A71 herbal medicine , Salvia miltiorrhiza ( Danshen ) , were screened for anti-EV-A71 .
We identified a natural product , rosmarinic acid ( RA ) , as a potential inhibitor of EV-A71 by cell-based antiviral assay and in vivo mouse model .
Results also show that RA may affect the early stage of viral infection and may @ @ @ @ @ @ @ with virus-P-selectin glycoprotein ligand-1 ( PSGL1 ) and virus-heparan sulfate interactions without abolishing the interaction between the virus and scavenger receptor B2 ( SCARB2 ) .
Sequencing of the plaque-purified RA-resistant viruses revealed a N104 K mutation in the five-fold axis of the structural protein VP1 , which contains positively charged amino acids reportedly associated with virus-PSGL1 and virus-heparan sulfate interactions via electrostatic attraction .
The plasmid-derived recombinant virus harbouring this mutation was confirmed tobe refractory to RA inhibition .
Receptor pull-down showed that this non-positively charged VP1-N104 is critical for virus binding @ @ @ @ @ @ @ residue is conserved among different EV-A71 strains , RA may be useful for inhibiting EV-A71 infection , even for emergent virus variants .
Our study provides insight into the molecular mechanism of virus-host interactions and identifies a promising new class of inhibitors based on its antiviral activity and broad spectrum effects against a range of EV-A71 .

Enterovirus A71 (EV-A71), a positive-stranded RNA virus of the Picornaviridae family, may cause neurological complications or fatality in children. We examined specific factors responsible for this virulence using a chemical genetics approach. Known compounds from an anti-EV-A71 herbal medicine, Salvia miltiorrhiza (Danshen), were screened for anti-EV-A71. We identified a natural product, rosmarinic acid (RA), as a potential inhibitor of EV-A71 by cell-based antiviral assay and in vivo mouse model. Results also show that RA may affect the early stage of viral infection and may target viral particles directly, thereby interfering with virus-P-selectin glycoprotein ligand-1 (PSGL1) and virus-heparan sulfate interactions without abolishing the interaction between the virus and scavenger receptor B2 (SCARB2). Sequencing of the plaque-purified RA-resistant viruses revealed a N104 K mutation in the five-fold axis of the structural protein VP1, which contains positively charged amino acids reportedly associated with virus-PSGL1 and virus-heparan sulfate interactions via electrostatic attraction. The plasmid-derived recombinant virus harbouring this mutation was confirmed tobe refractory to RA inhibition. Receptor pull-down showed that this non-positively charged VP1-N104 is critical for virus binding to heparan sulfate. As the VP1-N104 residue is conserved among different EV-A71 strains, RA may be useful for inhibiting EV-A71 infection, even for emergent virus variants. Our study provides insight into the molecular mechanism of virus-host interactions and identifies a promising new class of inhibitors based on its antiviral activity and broad spectrum effects against a range of EV-A71.


greenmedinfo--2020-05-14--R. canina methanolic extract consumption effectively protected against colonic histological/biochemi

R. canina methanolic extract consumption effectively protected against colonic histological/biochemical alterations induced by DSS intoxication.

is a well-known medicinal plant used in folk remedy that alleviates various disorders , including inflammation , gastritis , and @ @ @ @ @ this investigation was to identify and quantify the phenolic components ofmethanolic extract ( RCME ) @ @ @ @ @ action with dextran sulfate sodium ( DSS ) -generated mice colitis model .
RCME chemical @ @ @ @ @ Chromatography-Electrospray Ionization-Tandem Mass Spectrometry , and experimental animals received RCME at different doses before colitis @ @ @ @ @ during 7 days .
Another group received sulfasalazine as a positive control .
Colitis damages @ @ @ @ @ using histopathological and biochemical changes and improvements .
Many phenolic compounds have been identified .
@ @ @ @ @ intoxication induced an alteration of colonic epithelium associated with an oxidative stress state .
DSS @ @ @ @ @ or decrease of intracellular mediators such as free iron and ionizable calcium .
RCME consumption @ @ @ @ @ alterations induced by DSS intoxication providing support for the traditional use of this plant .

is a well-known medicinal plant used in folk remedy that alleviates various disorders, including inflammation, gastritis, and diarrhea. The objective of this investigation was to identify and quantify the phenolic components ofmethanolic extract (RCME) and to determine its protective action with dextran sulfate sodium (DSS)-generated mice colitis model. RCME chemical analysis was done using Liquid Chromatography-Electrospray Ionization-Tandem Mass Spectrometry, and experimental animals received RCME at different doses before colitis induction by oral DSS administration during 7 days. Another group received sulfasalazine as a positive control. Colitis damages and RCME benefits were assessed using histopathological and biochemical changes and improvements. Many phenolic compounds have been identified. In addition, the DSS intoxication induced an alteration of colonic epithelium associated with an oxidative stress state. DSS administration led to an increase or decrease of intracellular mediators such as free iron and ionizable calcium. RCME consumption effectively protected against colonic histological/biochemical alterations induced by DSS intoxication providing support for the traditional use of this plant.


greenmedinfo--2020-05-15--Topical application of wogonin provides a novel treatment of knee osteoarthritis.

Osteoarthritis ( OA ) is a degenerative joint disease characterized by inflammatory degradation of articular cartilage and subchondral bone .
Wogonin , a compound extracted from the plant ( colloquially known as skullcap ) , has previously been shown to have direct anti-inflammatory and antioxidative properties .
We examined the pain-reducing , anti-inflammatory , and chondroprotective effects of wogonin when applied as a topical cream .
We validated the efficacy of delivering wogonin transdermally in a cream using pig ear skin in a Franz diffusion system .
Using a surgical mouse model , we examined the severity and progression of @ @ @ @ @ @ @ of wogonin .
Using a running wheel to track activity , we found that mice with wogonin treatment were statistically more active than mice receiving vehicle treatment .
OA progression was analyzed using modified Mankin and OARSI scoring and direct quantification of cyst-like lesions at the chondro-osseus junction ; in each instance we observed a statistically significant attenuation of OA severity among mice treated with wogonin compared to the vehicle treatment .
Immunohistochemistry revealed a significant decrease in protein expression of transforming growth factorβ1 ( TGF-β1 ) , high temperature receptor A1 ( @ @ @ @ @ @ @ MMP-13 ) and NF-κB in wogonin-treated mice , further bolstering the cartilage morphology assessments in the form of a decrease in inflammatory and OA biomarkers .

Osteoarthritis (OA) is a degenerative joint disease characterized by inflammatory degradation of articular cartilage and subchondral bone. Wogonin, a compound extracted from the plant(colloquially known as skullcap), has previously been shown to have direct anti-inflammatory and antioxidative properties. We examined the pain-reducing, anti-inflammatory, and chondroprotective effects of wogonin when applied as a topical cream. We validated the efficacy of delivering wogonin transdermally in a cream using pig ear skin in a Franz diffusion system. Using a surgical mouse model, we examined the severity and progression of OA with and without the topical application of wogonin. Using a running wheel to track activity, we found that mice with wogonin treatment were statistically more active than mice receiving vehicle treatment. OA progression was analyzed using modified Mankin and OARSI scoring and direct quantification of cyst-like lesions at the chondro-osseus junction; in each instance we observed a statistically significant attenuation of OA severity among mice treated with wogonin compared to the vehicle treatment. Immunohistochemistry revealed a significant decrease in protein expression of transforming growth factorβ1 (TGF-β1), high temperature receptor A1 (HTRA1), matrix metalloprotease 13 (MMP-13) and NF-κB in wogonin-treated mice, further bolstering the cartilage morphology assessments in the form of a decrease in inflammatory and OA biomarkers.


greenmedinfo--2020-05-15--Wogonin may be a promising candidate for successful clinical management of osteosarcoma.

: Backgorund/Aim : Wogonin , a flavonoid-like compound extracted from the root of Scutellaria baicalensis Georgi , has been shown @ @ @ @ @ cancer cells .
Osteosarcoma is the most malignant type of bone cancer and can appear @ @ @ @ @ a high propensity for relapse and metastasis .
The present study aimed to assess the @ @ @ @ @ osteosarcoma stem cells .
MATERIALS AND METHODS : The cytotoxic effects of wogonin on CD133Cal72 @ @ @ @ @ through in vitro experiments by MTT assay , transwell assay , sphere-formation assay , flow @ @ @ @ @ blotting .
RESULTS : Wogonin suppressed stem cell characteristics and the expression of stem cell-related @ @ @ @ @ species ( ROS ) levels and ROS-related signaling of CD133Cal72 cells , effects which were @ @ @ @ @ .
CONCLUSION : Wogonin may be a promising candidate for successful clinical management of osteosarcoma @ @ @ @ @ stem cell-related genes .

: Backgorund/Aim: Wogonin, a flavonoid-like compound extracted from the root of Scutellaria baicalensis Georgi, has been shown to have anticancer effects against cancer cells. Osteosarcoma is the most malignant type of bone cancer and can appear in any bone, with a high propensity for relapse and metastasis. The present study aimed to assess the anticancer effects of wogonin on osteosarcoma stem cells.
MATERIALS AND METHODS: The cytotoxic effects of wogonin on CD133Cal72 osteosarcoma stem cells were assessed through in vitro experiments by MTT assay, transwell assay, sphere-formation assay, flow cytometry, immunocytochemistry and western blotting.
RESULTS: Wogonin suppressed stem cell characteristics and the expression of stem cell-related genes by regulating reactive oxygen species (ROS) levels and ROS-related signaling of CD133Cal72 cells, effects which were reversed by ROS scavenger N-acetylcysteine.
CONCLUSION: Wogonin may be a promising candidate for successful clinical management of osteosarcoma by regulating ROS-related mechanisms and stem cell-related genes.


greenmedinfo--2020-05-15--Naringin induces lysosomal permeabilization and autophagy cell death in AGS gastric cancer cells.

Autophagy is a process of active programmed cell death , where a dying cell induces autophagosomes and subsequently regulated by degradative machinery .
The aim of this study was to investigate the mechanism behind induction of autophagic cell death by Naringin flavonoid in AGS cancer cells .
Growth inhibition of AGS cells showed downregulation of PI3K/Akt/mTOR signaling by Naringin treatment .
Transmission electron microscopy observation showed swollen mitochondria and lysosome near peri-nuclear zone fused with autophagic vacuoles .
Rapamycin pre-treatment with Naringin showed significant decrease in mTOR phosphorylation and increase in LC3B activation in AGS cells .
Decrease in mTOR @ @ @ @ @ @ @ was observed by time-dependent treatment of Naringin .
Induction of lysosomal membrane permeabilization ( LMP ) was observed by LAMP1 activation leading lysosomal cell death by releasing Cathepsin D from lysosomal lumen to cytosol .
Naringin treated AGS cells showed up-regulating BH3 domain Bad , down-regulating Bcl-xL , and Bad phosphorylation and significant mitochondrial fluorescence intensity expression .
Significant localization of mitochondria and LC3B activation was examined by person coefficient correlation .
Activation of ERK1/2-p38 MAPKs and production of intracellular ROS has been observed over Naringin treatment .
It has also been elucidated @ @ @ @ @ @ @ , where ROS acted as upstream of ERK1/2-p38 MAPKs activation .
Lysosomal cell death involvement has been evaluated by BAF A1 pre-treatment , inhibiting LAMP1 , Cathepsin D , ROS , and blocking autophagolysosome in AGS cell death .
Taken together , these findings show that , Naringin induced autophagy cell death involves LMP mediated lysosomal damage and BH3 protein Bad activation in AGS cancer cells .

Autophagy is a process of active programmed cell death, where a dying cell induces autophagosomes and subsequently regulated by degradative machinery. The aim of this study was to investigate the mechanism behind induction of autophagic cell death by Naringin flavonoid in AGS cancer cells. Growth inhibition of AGS cells showed downregulation of PI3K/Akt/mTOR signaling by Naringin treatment. Transmission electron microscopy observation showed swollen mitochondria and lysosome near peri-nuclear zone fused with autophagic vacuoles. Rapamycin pre-treatment with Naringin showed significant decrease in mTOR phosphorylation and increase in LC3B activation in AGS cells. Decrease in mTOR phosphorylation is associated with lysosomal function activation was observed by time-dependent treatment of Naringin. Induction of lysosomal membrane permeabilization (LMP) was observed by LAMP1 activation leading lysosomal cell death by releasing Cathepsin D from lysosomal lumen to cytosol. Naringin treated AGS cells showed up-regulating BH3 domain Bad, down-regulating Bcl-xL, and Bad phosphorylation and significant mitochondrial fluorescence intensity expression. Significant localization of mitochondria and LC3B activation was examined by person coefficient correlation. Activation of ERK1/2-p38 MAPKs and production of intracellular ROS has been observed over Naringin treatment. It has also been elucidated that pre-treatment with NAC inhibited mitochondria-LC3B colocalization, where ROS acted as upstream of ERK1/2-p38 MAPKs activation. Lysosomal cell death involvement has been evaluated by BAF A1 pre-treatment, inhibiting LAMP1, Cathepsin D, ROS, and blocking autophagolysosome in AGS cell death. Taken together, these findings show that, Naringin induced autophagy cell death involves LMP mediated lysosomal damage and BH3 protein Bad activation in AGS cancer cells.


greenmedinfo--2020-05-15--Naringin induces endoplasmic reticulum stress-mediated apoptosis, inhibits β-catenin pathway and arr

Naringin induces endoplasmic reticulum stress-mediated apoptosis, inhibits β-catenin pathway and arrests cell cycle in cervical cancer cells.

Naringin is a promising anticancer bioflavonoid phytochemical , mainly extracted from citrus fruits .
This study evaluates the antiproliferative effect and the cell death mechanism induced by naringin on cervical cancer ( CC ) cells .
Our results demonstrated that naringin exerts significant inhibition in cell viability and exhibits IC50 value 745 , 764 , 793µM against C33A , SiHa , and HeLa cells respectively .
Annexin V FITC and immunoblotting analysis reveal significant apoptosis induction in cells exposed to higher doses naringin .
Mechanistically , naringin induces endoplasmic reticulum ( ER ) stress-associated cell killing in CC cells .
@ @ @ @ @ @ @ stress sensors , phosphorylates eIF2α by and activates apoptosis-associated protein CHOP and other associated proapoptotic proteins ( PARP1 and caspase-3 ) .
Intriguingly , pre-treatment with of ER stress inhibitor ( salubrinal ) , reverses the apoptotic effect exerted by naringin .
Additionally , the naringin abrogates the β-catenin pathway by decreasing the protein expression as well as phosphorylation of β-catenin ( Ser576 ) and GSK-3β ( Ser9 ) and simultaneously triggers cell cycle arrest at a G0/G1 phase by increasing the expression of cell cycle checkpoint proteins p21/cip and p27/kip .
Naringin @ @ @ @ @ @ @ Wnt/β-catenin signaling which eventually triggers the arrest of the cell cycle at a G0/G1 phase in CC cells .

Naringin is a promising anticancer bioflavonoid phytochemical, mainly extracted from citrus fruits. This study evaluates the antiproliferative effect and the cell death mechanism induced by naringin on cervical cancer (CC) cells. Our results demonstrated that naringin exerts significant inhibition in cell viability and exhibits IC50 value 745, 764, 793µM against C33A, SiHa, and HeLa cells respectively. Annexin V FITC and immunoblotting analysis reveal significant apoptosis induction in cells exposed to higher doses naringin. Mechanistically, naringin induces endoplasmic reticulum (ER) stress-associated cell killing in CC cells. Naringin increases the protein expression of ER stress sensors, phosphorylates eIF2α by and activates apoptosis-associated protein CHOP and other associated proapoptotic proteins (PARP1 and caspase-3). Intriguingly, pre-treatment with of ER stress inhibitor (salubrinal), reverses the apoptotic effect exerted by naringin. Additionally, the naringin abrogates the β-catenin pathway by decreasing the protein expression as well as phosphorylation of β-catenin (Ser576) and GSK-3β (Ser9) and simultaneously triggers cell cycle arrest at a G0/G1 phase by increasing the expression of cell cycle checkpoint proteins p21/cip and p27/kip. Naringin induces ER stress-mediated apoptosis and simultaneously abrogates Wnt/β-catenin signaling which eventually triggers the arrest of the cell cycle at a G0/G1 phase in CC cells.


greenmedinfo--2020-05-15--Naringin inhibits colorectal cancer cell growth.

In recent years , the incidence of colorectal cancer ( CRC ) has increased and research into new treatment methods for CRC has become a hot topic .
Naringin has an inhibitory effect on the PI3k/AKT/mTOR signaling pathway in various tumor cell types and the effect of naringin is closely related to the occurrence and proliferation of tumor cells .
The aim of this present study was to investigate whether naringin could inhibit the proliferation of CRC cells by inhibiting the PI3K/AKT/mTOR signaling pathway .
This could provide a more mechanism-based treatment for CRC .
MTT assays were used to @ @ @ @ @ @ @ with various concentrations of naringin .
The degree of apoptosis and the expression of apoptosis-related proteins ( Bcl-2 and Bax ) in CRC cells stimulated by naringin was detected using flow cytometry and western blot assays , respectively .
The expression levels of PI3K/AKT/mTOR-related proteins [ PI3K , AKT , mTOR , phosphorylated ( p ) -PI3K , p-AKT and p-mTOR ] after naringin stimulation in CRC cells were detected using western blot assays .
Naringin inhibited the proliferation of CRC cells in a dose-dependent manner .
Naringin promoted the apoptosis of CRC @ @ @ @ @ @ @ PI3K/AKT/mTOR signaling pathway in a dose-dependent manner .
The results demonstrated that naringin may be a promising therapeutic agent for the treatment of CRC , which may inhibit the proliferation of CRC cells and induce apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway .

In recent years, the incidence of colorectal cancer (CRC) has increased and research into new treatment methods for CRC has become a hot topic. Naringin has an inhibitory effect on the PI3k/AKT/mTOR signaling pathway in various tumor cell types and the effect of naringin is closely related to the occurrence and proliferation of tumor cells. The aim of this present study was to investigate whether naringin could inhibit the proliferation of CRC cells by inhibiting the PI3K/AKT/mTOR signaling pathway. This could provide a more mechanism-based treatment for CRC. MTT assays were used to detect the proliferation of CRC cells treated with various concentrations of naringin. The degree of apoptosis and the expression of apoptosis-related proteins (Bcl-2 and Bax) in CRC cells stimulated by naringin was detected using flow cytometry and western blot assays, respectively. The expression levels of PI3K/AKT/mTOR-related proteins [PI3K, AKT, mTOR, phosphorylated (p)-PI3K, p-AKT and p-mTOR] after naringin stimulation in CRC cells were detected using western blot assays. Naringin inhibited the proliferation of CRC cells in a dose-dependent manner. Naringin promoted the apoptosis of CRC cells and inhibited the activation of the PI3K/AKT/mTOR signaling pathway in a dose-dependent manner. The results demonstrated that naringin may be a promising therapeutic agent for the treatment of CRC, which may inhibit the proliferation of CRC cells and induce apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway.


greenmedinfo--2020-05-15--The genoprotective role of naringin.

The genoprotective role of naringin.

Since ancient times , fruits and edible plants have played a special role in the human diet for enhancing health and maintaining youthfulness .
The aim of our work was to determine the interactions between naringin , a natural ingredient of grapefruits , and DNA using an electrochemical biosensor .
Electrochemical methods allow analyzing the damages occurring in the structure of nucleic acids and their interactions with xenobiotics .
Our study showed that the changes in the location of electrochemical signals and their intensity resulted from the structural alterations in DNA .
The signal of adenine was affected at lower @ @ @ @ @ @ @ of guanine was unaffected in the same condition .
The dynamics of changes occurring in the peak height and surface of adenine related to naringin concentration was also significantly lower .
The complete binding of all adenine bases present in the tested double-stranded DNA solution was observed at naringin concentrations ranging from 8.5 to 10.0µM .
At larger concentrations , this active compound exerted an oxidizing effect on DNA .
However , the critical concentrations of naringin were found to be more than twice as high as the dose absorbable in an average @ @ @ @ @ @ @ results of our work might be helpful in the construction of electrochemical sensors for testing the content of polyphenols and would allow determining their genoprotective functionality .

Since ancient times, fruits and edible plants have played a special role in the human diet for enhancing health and maintaining youthfulness. The aim of our work was to determine the interactions between naringin, a natural ingredient of grapefruits, and DNA using an electrochemical biosensor. Electrochemical methods allow analyzing the damages occurring in the structure of nucleic acids and their interactions with xenobiotics. Our study showed that the changes in the location of electrochemical signals and their intensity resulted from the structural alterations in DNA. The signal of adenine was affected at lower concentrations of naringin, but the signal of guanine was unaffected in the same condition. The dynamics of changes occurring in the peak height and surface of adenine related to naringin concentration was also significantly lower. The complete binding of all adenine bases present in the tested double-stranded DNA solution was observed at naringin concentrations ranging from 8.5 to 10.0µM. At larger concentrations, this active compound exerted an oxidizing effect on DNA. However, the critical concentrations of naringin were found to be more than twice as high as the dose absorbable in an average human (4 µM). The results of our work might be helpful in the construction of electrochemical sensors for testing the content of polyphenols and would allow determining their genoprotective functionality.


greenmedinfo--2020-05-15--Naringenin regulates doxorubicin-induced liver dysfunction.

Doxorubicin ( Dox ) is an operational and largely used anticancer drug , used to treat an array of malignancies .
Nonetheless , its beneficial use is constrained due to its renal and hepatotoxicity dose dependently .
Numerous research findings favor the use of antioxidants may impact Dox-induced liver injury/damage .
In the current study , Wistar rats were given naringenin ( 50 and 100 mg/kg b.wt . )
orally for 20 days as prophylactic dose , against the hepatotoxicity induced by single intraperitoneal injection of Dox ( 20 mg/kg b.wt. )
.
Potency of naringenin against the liver damage @ @ @ @ @ @ @ malonyl aldehyde ( MDA ) as a by-product of lipid peroxidation , biochemical estimation of antioxidant enzyme system , reactive oxygen species ( ROS ) level , and inflammatory mediators .
Naringenin-attenuated ROS production , ROS-induced lipid peroxidation , and replenished reduced antioxidant armory , namely , catalase ( CAT ) , glutathione reductase ( GR ) , superoxide dismutase ( SOD ) , glutathione peroxidase ( GPx ) , and glutathione ( GSH ) .
Naringenin similarly diminished expression of Cox-2 and levels of NF-κB and other inflammatory molecules induced by the @ @ @ @ @ @ @ to the defensive effects of naringenin on Dox-induced liver damage .
The outcomes of the current study reveal that oxidative stress and inflammation are meticulously linked with Dox-triggered damage , and naringenin illustrates the potential effect on Dox-induced hepatotoxicity probably through diminishing the oxidative stress and inflammation .

Doxorubicin (Dox) is an operational and largely used anticancer drug, used to treat an array of malignancies. Nonetheless, its beneficial use is constrained due to its renal and hepatotoxicity dose dependently. Numerous research findings favor the use of antioxidants may impact Dox-induced liver injury/damage. In the current study, Wistar rats were given naringenin (50 and 100 mg/kg b.wt.) orally for 20 days as prophylactic dose, against the hepatotoxicity induced by single intraperitoneal injection of Dox (20 mg/kg b.wt.). Potency of naringenin against the liver damage caused by Dox was assessed by measuring malonyl aldehyde (MDA) as a by-product of lipid peroxidation, biochemical estimation of antioxidant enzyme system, reactive oxygen species (ROS) level, and inflammatory mediators. Naringenin-attenuated ROS production, ROS-induced lipid peroxidation, and replenished reduced antioxidant armory, namely, catalase (CAT), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH). Naringenin similarly diminished expression of Cox-2 and levels of NF-κB and other inflammatory molecules induced by the Dox treatment. Histology added further evidence to the defensive effects of naringenin on Dox-induced liver damage. The outcomes of the current study reveal that oxidative stress and inflammation are meticulously linked with Dox-triggered damage, and naringenin illustrates the potential effect on Dox-induced hepatotoxicity probably through diminishing the oxidative stress and inflammation.


greenmedinfo--2020-05-15--Naringenin could be used as a safe dietary supplement to protect against the toxicity and oxidative

Naringenin could be used as a safe dietary supplement to protect against the toxicity and oxidative stress associated with the use of Lambda-cyhalothrin.

BACKGROUND AND OBJECTIVES : Extensive use of Lambda-cyhalothrin ( LTC ) , a synthetic pyrethroid insecticide , has been associated with serious health problems to the non-target organisms including mammals .
The present study investigated the protective effect of naringenin ( NGN ) , an antioxidant flavonoid , against the toxicity induced LTC in the liver of male rats .
MATERIALS AND METHODS : Five groups of rats were assigned as follows ; control group , LTC group ( 6.12 mg kg-1 , 1/10 LD50 ) , LTC-NGN group ( 6.12 mg kg-1 LTC and 50 mg kg-1 NGN ) @ @ @ @ @ @ @ NGN and 6.12 mg kg-1 LTC ) and NGN group ( 50 mg kg-1 ) .
Doses were administrated orally for 21 consecutive days .
RESULTS : Administration of LTC induced liver damage as indicated by the increase in the activities of aspartate aminotransferase , alanine aminotransferase and alkaline phosphatase and in the level of total bilirubin in serum .
LTC also induced a significant elevation in the levels of serum total lipids , total cholesterol , triglycerides and low-density lipoproteins while high-density lipoproteins decreased .
Furthermore , LTC significantly disturbed the oxidant/antioxidant @ @ @ @ @ @ @ the elevation in lipid peroxidation , lipid hydroperoxides , protein carbonyl content and conjugated dienes with a concomitant inhibition in the major antioxidants such as reduced glutathione and the activities of superoxide dismutase , catalase , glutathione peroxidase , glutathione-S-transferase .
Both post-treatment and pre-treatment with NGN significantly modulated the LTC-induced hepatotoxicity and oxidative stress in rat 's liver and pretreatment was found to be more effective in improving most of the studied parameters in both serum and liver tissue .
CONCLUSION : NGN could be used as a safe dietary supplement to @ @ @ @ @ @ @ associated with the use of LTC .

BACKGROUND AND OBJECTIVES: Extensive use of Lambda-cyhalothrin (LTC), a synthetic pyrethroid insecticide, has been associated with serious health problems to the non-target organisms including mammals. The present study investigated the protective effect of naringenin (NGN), an antioxidant flavonoid, against the toxicity induced LTC in the liver of male rats.
MATERIALS AND METHODS: Five groups of rats were assigned as follows; control group, LTC group (6.12 mg kg-1, 1/10 LD50), LTC-NGN group (6.12 mg kg-1 LTC and 50 mg kg-1 NGN), NGN-LTC group (50 mg kg-1 NGN and 6.12 mg kg-1 LTC) and NGN group (50 mg kg-1). Doses were administrated orally for 21 consecutive days.
RESULTS: Administration of LTC induced liver damage as indicated by the increase in the activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase and in the level of total bilirubin in serum. LTC also induced a significant elevation in the levels of serum total lipids, total cholesterol, triglycerides and low-density lipoproteins while high-density lipoproteins decreased. Furthermore, LTC significantly disturbed the oxidant/antioxidant balance in the liver as shown by the elevation in lipid peroxidation, lipid hydroperoxides, protein carbonyl content and conjugated dienes with a concomitant inhibition in the major antioxidants such as reduced glutathione and the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase. Both post-treatment and pre-treatment with NGN significantly modulated the LTC-induced hepatotoxicity and oxidative stress in rat's liver and pretreatment was found to be more effective in improving most of the studied parameters in both serum and liver tissue.
CONCLUSION: NGN could be used as a safe dietary supplement to protect against the toxicity and oxidative stress associated with the use of LTC.


greenmedinfo--2020-05-15--Naringenin ameliorates diabetic neuropathic pain by modulation of oxidative-nitrosative stress, cyto

Naringenin ameliorates diabetic neuropathic pain by modulation of oxidative-nitrosative stress, cytokines and MMP-9 levels.

Diabetes mellitus is a serious debilitating epidemic affecting all social strata , imposing huge health , social and economic burdens .
Diabetic neuropathic pain , an important microvascular complication of diabetes mellitus , characterized by allodynia and hyperalgesia , is recognized as one of the most difficult types of pain to treat .
The development of tolerance , inadequate relief and potential toxicity of classical antinociceptives warrant the investigation of newer agents to relieve this pain .
Reactive oxygen/nitrogen species , cytokines and matrix metalloproteinases ( MMPs ) are implicated in the pathogenesis of diabetic neuropathy .
The present study @ @ @ @ @ @ @ naringenin , a citrus flavonoid , on streptozotocin induced diabetic neuropathic pain in Wistar rats .
After 8 weeks of diabetes induction , rats developed neuropathy which was evident from marked hyperalgesia and allodynia associated with enhanced oxidative-nitrosative stress , release of inflammatory mediators ( TNF-α , TGF-1β ) , MMP-9 activation and decreased motor nerve conduction velocity .
Treatment with naringenin ( 25 , 50 , 100 mg kg-1 ) for 4 weeks starting from the 5th week of streptozotocin injection significantly attenuated behavioral , biochemical and molecular changes , along with @ @ @ @ @ @ @ a dose-dependent manner .
Moreover , diabetic rats treated with insulin-naringenin combination produced a more pronounced effect as compared to individual drugs .
The major finding of the study is that insulin alone corrected the hyperglycemia and partially reversed the pain response in diabetic rats .
However , combination with naringenin not only attenuated the diabetic condition but also reversed neuropathic pain through modulation of oxidative-nitrosative stress , inflammatory cytokine release and MMP inhibition in the diabetic rats .
Modulation of MMP-9 by a natural flavonoid like naringenin seems to be a novel @ @ @ @ @ @ @

Diabetes mellitus is a serious debilitating epidemic affecting all social strata, imposing huge health, social and economic burdens. Diabetic neuropathic pain, an important microvascular complication of diabetes mellitus, characterized by allodynia and hyperalgesia, is recognized as one of the most difficult types of pain to treat. The development of tolerance, inadequate relief and potential toxicity of classical antinociceptives warrant the investigation of newer agents to relieve this pain. Reactive oxygen/nitrogen species, cytokines and matrix metalloproteinases (MMPs) are implicated in the pathogenesis of diabetic neuropathy. The present study was designed to explore the effect of naringenin, a citrus flavonoid, on streptozotocin induced diabetic neuropathic pain in Wistar rats. After 8 weeks of diabetes induction, rats developed neuropathy which was evident from marked hyperalgesia and allodynia associated with enhanced oxidative-nitrosative stress, release of inflammatory mediators (TNF-α, TGF-1β), MMP-9 activation and decreased motor nerve conduction velocity. Treatment with naringenin (25, 50, 100 mg kg-1) for 4 weeks starting from the 5th week of streptozotocin injection significantly attenuated behavioral, biochemical and molecular changes, along with alterations in motor nerve conduction velocity in a dose-dependent manner. Moreover, diabetic rats treated with insulin-naringenin combination produced a more pronounced effect as compared to individual drugs. The major finding of the study is that insulin alone corrected the hyperglycemia and partially reversed the pain response in diabetic rats. However, combination with naringenin not only attenuated the diabetic condition but also reversed neuropathic pain through modulation of oxidative-nitrosative stress, inflammatory cytokine release and MMP inhibition in the diabetic rats. Modulation of MMP-9 by a natural flavonoid like naringenin seems to be a novel approach to target diabetic neuropathic pain.


greenmedinfo--2020-05-15--Citrus Lemon essential oil has the potential to be used as a safe cell-depended anticancer agent for

Citrus Lemon essential oil has the potential to be used as a safe cell-depended anticancer agent for human lung cancer.

essential oil ( CLEO ) has been introduced as a strong antioxidant mixture .
However , it is not efficient @ @ @ @ @ nature .
Nanoemulsions improve the drugs ' bio-compatibility in aqueous conditions.The CLEO nanoemulsion ( CLEO-NE @ @ @ @ @ and they were characterized .
The anti-angiogenic and antioxidant activities were studied by the chicken @ @ @ @ @ and antioxidant ( ABTS and DPPH ) assays , respectively .
Finally , the apoptotic @ @ @ @ @ HFF and A549 was evaluated by [ 3- ( 4,5-Dimethylthiazol-2-yl ) -2,5-Diphenyltetrazolium Bromide ] ( @ @ @ @ @ time-PCR ( measuring Cas-3 gene expression ) .The 30.2-nm CLEO-NE droplets significantly increased Cas-3 in @ @ @ @ @ in chick embryo chorioallantoic membrane ( p < 0.01 ) .In conclusion , CLEO-NE has @ @ @ @ @ as a safe cell-depended anticancer agent for human lung cancer .
However , further genes @ @ @ @ @ be studied to clarify its targeted-anticancer activity .

essential oil (CLEO) has been introduced as a strong antioxidant mixture. However, it is not efficient enough due to its hydrophobic nature. Nanoemulsions improve the drugs' bio-compatibility in aqueous conditions.The CLEO nanoemulsion (CLEO-NE) was formulated by ultrasound-based-emulsification and they were characterized. The anti-angiogenic and antioxidant activities were studied by the chicken chorioallantoic membrane (CAM) and antioxidant (ABTS and DPPH) assays, respectively. Finally, the apoptotic property of CLEO-NE on both HFF and A549 was evaluated by [3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide] (MTT) assay and Real time-PCR (measuring Cas-3 gene expression).The 30.2-nm CLEO-NE droplets significantly increased Cas-3 in A549 cells and decreased angiogenesis in chick embryo chorioallantoic membrane (p<0.01).In conclusion, CLEO-NE has the potential to be used as a safe cell-depended anticancer agent for human lung cancer. However, further genes and cell lines have to be studied to clarify its targeted-anticancer activity.


greenmedinfo--2020-05-15--Antibacterial activity of Rosmarinus officinalis, Zingiber officinale, Citrus aurantium bergamia, an

Antibacterial activity of Rosmarinus officinalis, Zingiber officinale, Citrus aurantium bergamia, and Copaifera officinalis against Enterococcus faecalis.

This study aimed to evaluate the efficacy of different concentrations of essential oils combined with calcium hydroxide against .
Thirteen experimental groups were formed : NC ( negative control ) ; PC ( positive control ) ; GC ( growth control ) ; SC ( sterilization control ) ; RO ( ) ; ROH ( calcium hydroxide + RO ) ; ZO ( ) ; ZOH ( calcium hydroxide + ZO ) ; AB ( ) ; ABH ( calcium hydroxide + AB ) ; CO ( ) ; COH ( calcium hydroxide + CO ) ; DWH ( calcium @ @ @ @ @ @ @ reconstitution of thestrain , microdilution testing was performed to define the minimum inhibitory concentration ( MIC ) and minimum bactericidal concentration ( MBC ) .
The data were tabulated in an Excel spreadsheet , and the MIC and MBC were calculated in accordance with the Bacteriological Analytical Handbook .
MICs in the range of 0 to 100 mg/ml were only observed in the ROH group .
The RO , ROH , AB , ZO , and ZOH presented absolute data for MBC .
Bacterial growth was detected in the DWH group at all @ @ @ @ @ @ @ essential oils tested here with calcium hydroxide appears promising as an intracanal medication in endodontic treatment because of its effectiveness against .
Essential oils are important in endodontic therapy since calcium hydroxide , the gold standard intracanal medication , is not effective against .

This study aimed to evaluate the efficacy of different concentrations of essential oils combined with calcium hydroxide against. Thirteen experimental groups were formed: NC (negative control); PC (positive control); GC (growth control); SC (sterilization control); RO (); ROH (calcium hydroxide + RO); ZO (); ZOH (calcium hydroxide + ZO); AB (); ABH (calcium hydroxide + AB); CO (); COH (calcium hydroxide + CO); DWH (calcium hydroxide and distilled water). After reconstitution of thestrain, microdilution testing was performed to define the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). The data were tabulated in an Excel spreadsheet, and the MIC and MBC were calculated in accordance with the Bacteriological Analytical Handbook. MICs in the range of 0 to 100 mg/ml were only observed in the ROH group. The RO, ROH, AB, ZO, and ZOH presented absolute data for MBC. Bacterial growth was detected in the DWH group at all concentrations tested. The combination of the essential oils tested here with calcium hydroxide appears promising as an intracanal medication in endodontic treatment because of its effectiveness against. Essential oils are important in endodontic therapy since calcium hydroxide, the gold standard intracanal medication, is not effective against.


greenmedinfo--2020-05-15--Genomic instability decreases in HIV patient by complementary therapy with Rosmarinus officinalis ex

Genomic instability decreases in HIV patient by complementary therapy with Rosmarinus officinalis extracts.

Genomic instability is associated with increased oxidative stress in patients with human immunodeficiency virus ( HIV ) .
The aim @ @ @ @ @ determine the effect of intake of methanolic and aqueous extractson genomic instability in HIV patients @ @ @ @ @ patients under pharmacological treatment with ATRIPLA who were divided into three groups : group 1 @ @ @ @ @ therapy ; group 2 , patients with ATRIPLA and rosemary aqueous extract ( 4 g/L @ @ @ @ @ group 3 , patients with ATRIPLA and rosemary methanolic extract ( 400 mg/day ) .
@ @ @ @ @ through the buccal micronucleus cytome assay .
Oral epithelial cells were taken at the beginning @ @ @ @ @ later .
The groups that received the pharmacological therapy with ATRIPLA and the complementary therapy @ @ @ @ @ the number of cells with micronuclei and nuclear abnormalities compared with the group that only @ @ @ @ @ therapy withdecreased the genomic instability in HIV patients .

Genomic instability is associated with increased oxidative stress in patients with human immunodeficiency virus (HIV). The aim of this study was to determine the effect of intake of methanolic and aqueous extractson genomic instability in HIV patients. We studied 67 HIV patients under pharmacological treatment with ATRIPLA who were divided into three groups: group 1, patients under ATRIPLA antiretroviral therapy; group 2, patients with ATRIPLA and rosemary aqueous extract (4 g/L per day); and group 3, patients with ATRIPLA and rosemary methanolic extract (400 mg/day). The genomic instability was evaluated through the buccal micronucleus cytome assay. Oral epithelial cells were taken at the beginning and 1 and 4 months later. The groups that received the pharmacological therapy with ATRIPLA and the complementary therapy withextracts showed a decrease in the number of cells with micronuclei and nuclear abnormalities compared with the group that only received ATRIPLA. The complementary therapy withdecreased the genomic instability in HIV patients.


greenmedinfo--2020-05-15--Pre-treatment with evening primrose oil showed significant antioxidant, anti-inflammatory, and genop

Pre-treatment with evening primrose oil showed significant antioxidant, anti-inflammatory, and genoprotective effects against the toxic effects of cyclophosphamide.

Cyclophosphamide ( CP ) is a well-known antineoplastic agent ; however , its clinical use can be associated with various organ toxicities .
Evening primrose oil ( EPO ) contains several phytoconstituents with potent anti-oxidant and anti-inflammatory activities .
This experimental study was performed to investigate the chemoprotective effects of EPO in the liver and pancreas of CP-intoxicated mice .
Thirty-two albino mice were randomly divided into 4 equal groups : group I received saline ( control mice ) , group II were treated with CP at 100 mg/kg/day for two subsequent days , and groups III and VI were @ @ @ @ @ @ @ EPO , respectively for 14 days , followed by two doses of CP at the 15th and 16th days of the experiment .
Then , mice were sacrificed and histopathological examinations , biochemical studies , and DNA laddering tests were conducted for hepatic and pancreatic tissues .
Cyclophosphamide-intoxicated mice showed significant increases ( < 0.05 ) in the serum levels of liver enzymes , pancreatic amylase and tissue levels of malondialdehyde , and TNF-α , as well as a significant decrease ( < 0.05 ) in the serum insulin level .
In addition @ @ @ @ @ @ @ disturbed tissue architecture , hydropic degeneration , congested vessels , and inflammatory infiltrates , as well as increased DNA fragmentation .
In a dose-dependent manner , pretreatment with EPO was associated with significant improvements ( < 0.05 ) in all biochemical parameters and significant amelioration of histopathological alterations and DNA fragmentation in CP-intoxicated mice .
Pretreatment with EPO showed significant antioxidant , anti-inflammatory , and genoprotective effects against the toxic effects of CP in mice hepatic and pancreatic tissues .

Cyclophosphamide (CP) is a well-known antineoplastic agent; however, its clinical use can be associated with various organ toxicities. Evening primrose oil (EPO) contains several phytoconstituents with potent anti-oxidant and anti-inflammatory activities. This experimental study was performed to investigate the chemoprotective effects of EPO in the liver and pancreas of CP-intoxicated mice. Thirty-two albino mice were randomly divided into 4 equal groups: group I received saline (control mice), group II were treated with CP at 100 mg/kg/day for two subsequent days, and groups III and VI were treated with 5 and 10 mg/kg/day bw EPO, respectively for 14 days, followed by two doses of CP at the 15th and 16th days of the experiment. Then, mice were sacrificed and histopathological examinations, biochemical studies, and DNA laddering tests were conducted for hepatic and pancreatic tissues. Cyclophosphamide-intoxicated mice showed significant increases (<0.05) in the serum levels of liver enzymes, pancreatic amylase and tissue levels of malondialdehyde, and TNF-α, as well as a significant decrease (<0.05) in the serum insulin level. In addition, both hepatic and pancreatic tissues showed disturbed tissue architecture, hydropic degeneration, congested vessels, and inflammatory infiltrates, as well as increased DNA fragmentation. In a dose-dependent manner, pretreatment with EPO was associated with significant improvements (<0.05) in all biochemical parameters and significant amelioration of histopathological alterations and DNA fragmentation in CP-intoxicated mice. Pretreatment with EPO showed significant antioxidant, anti-inflammatory, and genoprotective effects against the toxic effects of CP in mice hepatic and pancreatic tissues.