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The Prevention Of Emodin And Berberine In Nonalcoholic Fatty Liver Disease

Posted on:2010-12-08Degree:MasterType:Thesis
Country:ChinaCandidate:H L WangFull Text:PDF
GTID:2144360275961432Subject:Digestive science
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Objective insulin resistance(IR) is the pathophysiologic foundation of nonalcoholic fatty liver disease (NAFLD). Improving IR is very important role in prevention of NAFLD. Emodin and berberine are separately main active ingredients of Rhubarb and Coptis, with the improvement of IR. This experiment aims to study on the mechanism of IR for HepG2 cells induced by high concentrations of free fatty acid (FFA) and the prevention effect of emodin and berberine. It would provide new methods and ideas for the prevention and treatment of NAFLD.Methods The model of IR was established with HepG2 cells cultured at high concentrations of FFA,the glucose contents and hepatic glycogen contents were measured. The optimal concentration of emodin and berberine were determined by MTT.The expression of adiponectin receptor2 (AdipoR2)mRNA,peroxisome proliferator-activated receptor gamma (PPARγ)mRNA and phosphoenolpyruvate carboxykinase (PEPCK) mRNA in HepG2 cell were detected by RT-PCR.Results (一) MTT experiments showed that the cell survival rate with the concentration of 10μmol / L emodin is 92.5%..The cell survival rate with the concentration of 10μmol / L berberine is 90.3%. Therefore, we selected 10μmol / L for the experimental concentration of emodin and berberine.(二)Prevention Group 1. The glucose contents in IR model group was obviously higher than those in normal group (P <0.01). The glucose contents was significantly lower compared with IR model group when emodin and FFA or berberine and FFA were simultaneously added in culture medium.It was considered no statistical difference compared with control group.2.Hepatic glycogen contents in IR model group was lower than control group.But the hepatic glycogen contents in both drug groups higher than model group.3. The expression of AdipoR2Mrna, PPARγmRNA and PEPCKmRNA were detected in normal HepG2 cells . The expression of AdipoR2 and PPARγmRNA strongly reduced in model group of IR.But the expression of PEPCKmRNA were significantly higher than those in controlgroup.Th- -e expression of AdipoR2mRNAd and PPARγmRNA were increased as emodin and FFA or berberine and FFA were simultaneously added in culture medium,But the expression of PEPCKmRNA was decreased.(三) Treatment group :1.The glucose contents in culture medium and the expression of PEPCKmRNA in model group were significantly higher than those in control group ,but hepatic glycogen contents and the expression of AdipoR2 and PPARγmRNA strongly reduced in model group of IR( P < 0.01).2.The effect of improving IR could be obvious as emodin(10μmol/L)or berberine(10μmol/L)or pioglitazone(10μmol/L)was respectively added in culture medium.It was discovered that the glucose contents in culture medium and the expression of PEPCKmRNA after adding these drugs were significantly lower than model group. But the hepatic glycogen contents and the expression of AdipoR2mRNA and PPARγmRNA increased. And there was no statistical difference that three groups respectively compared with the normal group(P>0.01) .Conclusions These results suggest that HepG2 cells cultured at high concentrations of FFA,could successfully induce hepatic IR. Emodin berberine and pioglitazone can respectively improve IR,which may be resulted from AdipoR2,PPARγand PEPCK.So it would provide new methods and ideas for the prevention and treatment of NAFLD.
Keywords/Search Tags:Insulin resistance, Emodin, Berberine, AdipoR2
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