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作 者:杨文卓[1] 曾民德[1] 范竹萍[1] 茅益民 陆伦根[1] 曹爱平[1]
出 处:《中华消化杂志》2003年第3期165-168,共4页Chinese Journal of Digestion
摘 要:目的 观察氧化苦参碱预防及治疗大鼠肝纤维化的疗效并探讨其作用机制。方法 采用二甲基亚硝胺诱导的大鼠肝纤维化模型 ,观察氧化苦参碱 (30mg/kg、90mg/kg)干预前后肝指数、血及肝组织生化、羟脯氨酸含量、肿瘤坏死因子 (TGF) β1mRNA表达水平、电镜及病理组织学改变。结果 氧化苦参碱干预组较模型组丙氨酸转氨酶、天冬氨酸转氨酶下降 ,肝组织羟脯氨酸含量及TGF β1mR NA表达水平降低 (P <0 .0 1) ;干预组肝组织内超氧化物歧化酶、谷胱甘肽过氧化物酶较模型组升高 ,而丙二醛低于模型组 ;电镜显示肝细胞损伤减轻 ,病理组织学改善。结论 氧化苦参碱对二甲基亚硝胺诱导的肝纤维化有预防及治疗作用 ,其部分机制为通过抗脂质过氧化而保护肝细胞。Objective To investigate the prophylactic and therapeutic effect of oxymatrine(OM) on experimental liver fibrosis and to reveal its mechanism. Methods By establishing models of dimethylnitrosamine(DMN) induced liver fibrosis in rats, we observed the effect of oxymatrine on liver/weight index, serum and tissue biochemical indexes, content of liver hydroxyproline, expression of TGFβ1 mRNA, electromicroscopic changes and tissue pathology. Results There was a decline of serum AST, ALT and liver hydroxyproline in oxymatrine group, compared to those of the DMN group( P < 0.01). Liver superoxide dismutes(SOD), glutathione peroxidase(GST PX) was higher in OM intervention group than in model group, while malodialdehyde(MDA) was reduced. RT PCR revealed the expression of TGFβ1 mRNA in OM group was lower than that in model group. Electromicroscopy show that OM groups had milder hepatocyte degeneration and less fibrosis accumulation than model group. Microscopy revealed there was wide septa expansion from portal area to central venous, piecemeal and confluent necrosis and there was pseudo nodular formation in part of the lobular in model group, while in OM group these lesions were much improved. Conclusions Our results suggest OM has prophylacitc and therapeutic effects in DMN induced rat liver fibrosis, probably by protecting hepatocyte and suppressing fibrosis accumulation through its anti lipoperoxidation.
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