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机构地区:[1]辽宁广播电视大学,辽宁沈阳110034 [2]沈阳药科大学生命科学与生物制药学院,辽宁沈阳110016 [3]辽宁中医药大学附属第三医院,辽宁沈阳110005
出 处:《中国现代医学杂志》2014年第2期24-28,共5页China Journal of Modern Medicine
基 金:辽宁省教育厅资助项目(No:L2010525)
摘 要:目的观察丹酚酸B对四氯化碳(CCl4)诱导的大鼠肝纤维化的防治作用。方法采用CCl4诱导的大鼠肝纤维化模型,分为正常组、对照组、丹酚酸B低剂量及高剂量组。检测大鼠血清肝功能指标、肝组织氧化应激指标、肝组织病理及胶原沉积情况;应用酶联免疫吸附(ELISA)方法检测转化生长因子-β1(TGF-β1)含量。结果对照组大鼠血清ALT、AST显著升高,治疗组显著下降;治疗组大鼠肝脏胶原纤维沉积明显减少;对照组大鼠肝组织SOD活性及GSH含量明显降低,MDA和TGF-β1含量显著升高;治疗组大鼠肝组织SOD活性及GSH含量有所升高,MDA和TGF-β1含量降低。结论丹酚酸B具有抗CCl4诱导的大鼠肝纤维化及氧化损伤的作用。[Objective] To investigate the effects of salvianolic acid B (Sal B) on liver fibrosis induced by carbon tetrachloride (CCh) in rats. [Methods] Rats were divided into normal, model control, low-dose and high-dose Sal B groups. Serum samples were collected for liver function tests. Liver tissues were harvested tot intrahepatic reactive oxygen species detection. Histological changes and collagen deposition were observed in H&E and Sirius-red staining sections. The expression of TGF-β1 were analyzed by ELISA. [Results] Serum ALT and AST and hepatic MDA, TGF-β1 increased significantly in model control gruup. After Sal B adminis- tration, serum ALT, AST and hepatic TGF-β1 were inhibited significantly. Histological detection showed that collagen deposition was observed in the liver in model control group and these pathological changes were al- leviated by Sal B. On the other hand, hepatic SOD and GSH decreased in model control group. Sal B in- creased hepatic SOD and improved hepatic GSH. [Conclusion] Sal B can inhibit liver fibrosis induced by CCl4.
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