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Aim To explore the effects of mangiferin on tissue factor(TF) expression in human umbilical vein endothelial cells(HUVECs) and the underlying mechanisms.Methods HUVECs were isolated and primarily cultured in vitro.After the treatment with mangiferin and oxidized low density lipoprotein(oxLDL), TF expression was determined in HUVECs with real-time PCR and Western blot.Results oxLDLinduced the mRNA and protein expression and pro-thrombotic activity of TF in HUVECs.However, the inductive effects of oxLDL were blocked significantly by mangiferin.Furthermore, mangiferin modified TF expression and activity in a dose-dependent manner.Mangiferin was demonstrated to enhance the activity of peroxisome proliferator-activated receptor gamma(PPARγ).In contrast, GW9662, an antagonist of PPARγ, reversed at least partially the suppressive effects of mangiferin on TF.Conclusion Through activating PPARγ, mangiferin suppresses the expression of TF serving pro-thrombotic functions in endothelial cells.
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Objective To observe the clinical effect of magnesium isoglycyrrhizinate on moderate and severe nonalcoholic steatohepatitis(NASH) and analyse its mechanism. Methods 42 cases with moderate and severe nonalcoholic steatohepatitis were selected in our study. All patients were divided into observation group and control group randomly. Control group were received simvastatin while the observation group were received simvastatin combined with magnesium isoglycyrrhizinate treatment. The course was 6 weeks.The changes of NASH classiifcation, clinical symptom, liver function, lipid levels and liver ifbrosis items in two groups before and after treatment were observed and recorded. Results All patients were received 6 week treatment, none of them dropped out. The clinical symptoms were improved in both two groups. There were 5 severe NASH improved to moderate NASH, 8 moderate NASH improved to mild NASH in observation group while only 3 severe NASH improved to moderate NASH in control group. The difference of NASH classiifcation between two groups was signiifcant(P<0.05). Compared to pre-treatment, the AST, ALT, TBIL,γ-GT were decreased in both two groups. But the liver function items in observation were lower than control group(P<0.05). The lipid level were decreased in both two group and there were no signiifcant differences between two groups after treatment. The level of PC III, HA, C-IV were decreased in observation group while had no changes in control group. Conclusion The magnesium isoglycyrrhizinate could decrease the AST, ALT and lipid level, improve the classiifcation of liver ifbrosis, and had low rate of side effect during treatment.
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Objective To investigate the protective effects of α-lipoic acid in rats with acute panereatitis(AP)and its potential mechanism.Methods Wistar rats were randomly divided into four groups according to random number table:sham operation(SO)group,AP group,normal saline(NS)group and α- lipoic acid group with 30 rats in each group.AP model was induced by retrograde iniection of 3.5%sodium taurocholate into the pancreatobiliary duct.Rats in α-lipoic acid group immediately received α-lipoic acid intra- peritoneal injection at the dose of 1 mg/kg.Rats in NS group received sanle amount of normal saline.The rats were sacrificed at 1,3,6,9 and 12 h after AP induction.The serunl levels of amylase.TNF-α and ICAM-1 were measured.Pancreatic histological changes were observed.The activities of pancreatic SOD and MDA were measured. Results In rats of AP group,optical microscopy showed pancreatic edema,adhesion and necrosis. The semm amylase,TNF-α,ICAM-1 and MDA levels in pancreatic tissue 6h after operalion were(2211±547)U/L,(174.8±7.9)ng/ml,(49.3±8.0)ng/ml and(32.2±5.9)U/mg prot,respectively,in AP group;which were significantly increased when compared with those of SO group(P<0.05).Pancreatic SOD activity was(38.5±9.5)U/mg prot,which was signifieandy lower than(56.7±6.7)U/mg pint of SO group (p<0.05).The serum amylase,TNF-α,ICAM-1 and MDA levels in pancreatic tissue 6 h after operation in α-lipoic acid group were(1478±642)U/L,(164.8±6.2)ng/ml,(37.5±3.9)ng/ml and(20.2 ±8.4)U/mg prot,respectively;which were significantly decreased when compared with those of AP group(P<0.05).Pancreatic SOD activity was(66.0±8.6)U/mg prot,which were significantly hisher than(38.5±9.5)U/mg prot of AP group(P<0.05).Condusiors The pathogenesis of AP wag associated with oxiddative stress,and α-lipoic acid as an antioxidant played a role in the treatment of AP.the possiblemechanismsincludedinhibitedproduction of TNF-α and ICAM-1.