Therapeutic effect of 17β-estradiol on multiple hepatotoxic factors-induced liver fibrosis in rats
Jie Ping
Abstract
Jie Ping
Abstract
Objective To investigate the therapeutic effect and mechanism of 17β-Est on multiple hepatotoxic factors-induced liver fibrosis in rats.Methods The liver fibrotic model in rats was induced by multiple hepatotoxic factors,including carbon tetrachloride,ethanol and high fat/low proteins for 4 weeks.After completing models,the treatment groups were administered 17β-Est(1,2mg/kg) through intraperitoneal injection,daily for 3 days.The hydroxyproline(Hyp) was determined.Liver biopsies were obtained for histological.Meanwhile,the expression of matrix metalloproteinases-2(MMP-2) in liver was analyzed by Western blot.Results Compared with the fibrotic model control,contents of hepatic Hyp were decreased by 17β-Est treatment.Histopathological changes,especially myofibroblast proliferation,were reduced in 17β-Est-treated groups.Conclusion 17β-Est could effectively prevent rats from experimental liver fibrosis through enhancing the activity of MMPs,promoting degradation of extracellular matrix(ECM).
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Objective To investigate the therapeutic effect and mechanism of 17β-Est on multiple hepatotoxic factors-induced liver fibrosis in rats.Methods The liver fibrotic model in rats was induced by multiple hepatotoxic factors,including carbon tetrachloride,ethanol and high fat/low proteins for 4 weeks.After completing models,the treatment groups were administered 17β-Est(1,2mg/kg) through intraperitoneal injection,daily for 3 days.The hydroxyproline(Hyp) was determined.Liver biopsies were obtained for histological.Meanwhile,the expression of matrix metalloproteinases-2(MMP-2) in liver was analyzed by Western blot.Results Compared with the fibrotic model control,contents of hepatic Hyp were decreased by 17β-Est treatment.Histopathological changes,especially myofibroblast proliferation,were reduced in 17β-Est-treated groups.Conclusion 17β-Est could effectively prevent rats from experimental liver fibrosis through enhancing the activity of MMPs,promoting degradation of extracellular matrix(ECM).
Key concepts: Medicine, Hydroxyproline, Carbon tetrachloride, Matrix metalloproteinase, Extracellular matrix, CCL4, Western blot, Liver fibrosis