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丹酚酸B盐对二甲基亚硝胺诱导的肝纤维化大鼠肝脏转化生长因子β1及其受体蛋白表达的影响
引用本文:王晓柠,胡义扬,刘成海,刘平,朱大元.丹酚酸B盐对二甲基亚硝胺诱导的肝纤维化大鼠肝脏转化生长因子β1及其受体蛋白表达的影响[J].中西医结合学报,2005,3(4):286-289.
作者姓名:王晓柠  胡义扬  刘成海  刘平  朱大元
作者单位:1. 上海中医药大学肝病研究所,上海中医药大学曙光医院,上海,201203
2. 中国科学院上海药物研究所,上海,201203
摘    要:目的:研究中药丹参的有效成分丹酚酸B盐抗肝纤维化作用的机制.方法:Wistar大鼠24只随机分为正常对照组、模型组和丹酚酸B盐治疗组.采用二甲基亚硝胺诱导大鼠肝纤维化模型,丹酚酸B盐治疗组在造模4周后给予丹酚酸B盐治疗4周.治疗结束后,用盐酸水解法检测全部大鼠肝组织中羟脯氨酸的含量,用Western印迹法检测肝组织Ⅰ型胶原蛋白、转化生长因子β1(transforming growth factor-beta1,TGF-β1)、转化生长因子β受体Ⅰ(transforming growth factor-beta receptor type Ⅰ,TβRⅠ)、转化生长因子β受体Ⅱ(transforming growth factor-beta receptor type Ⅱ,TβRⅡ)蛋白的表达.结果:模型组大鼠肝组织中羟脯氨酸的含量、Ⅰ型胶原蛋白、TGF-β1及其受体TβRⅠ和TβRⅡ蛋白的表达较正常对照组均有显著增加,而丹酚酸B盐治疗组的上述指标与模型组比较则均有不同程度的下降.结论:丹酚酸B盐具有明显的抗肝纤维化作用,其作用机制与抑制TGF-β1及其受体蛋白的表达有关.

关 键 词:肝纤维化  丹酚酸B盐  二甲基亚硝胺  TGF-β1  受体
文章编号:1672-1997(2005)04-0286-04
收稿时间:2005-03-18
修稿时间:2005年3月18日

Effects of salvianolic acid B on expressions of TGF-β1 and its receptors in liver of rats with dimethylnitrosamine-induced hepatic fibrosis
WANG Xiao-Ning,HU Yi-yang,LIU Cheng-hai,LIU Ping,ZHU Da-Yuan.Effects of salvianolic acid B on expressions of TGF-β1 and its receptors in liver of rats with dimethylnitrosamine-induced hepatic fibrosis[J].Journal of Chinese Integrative Medicine,2005,3(4):286-289.
Authors:WANG Xiao-Ning  HU Yi-yang  LIU Cheng-hai  LIU Ping  ZHU Da-Yuan
Institution:Institute of Liver Diseases, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Abstract:OBJECTIVE: To study the therapeutic mechanism of salvianolic acid B (SA-B) in treating hepatic fibrosis. METHODS: Twenty-four Wistar rats were randomly divided into 3 groups: normal control group, untreated group and SA-B-treated group. Rats in the untreated and SA-B-treated groups were injected intraperitoneally with 0.5% dimethylnitrosamine (DMN) for 4 weeks, daily for 3 days each week at a dose of 10 microg/kg, to induce hepatic fibrosis. Then, rats in the SA-B-treated group were given SA-B orally for another 4 weeks. Hydroxyproline (Hyp) contents in liver tissue of the rats in 3 groups were determined with HCl hydrolysis, and collagen type I, transforming growth factor-beta 1 (TGF-beta1), transforming growth factor-beta receptor type I (TbetaRI) and transforming growth factor-beta receptor type II (TbetaRII) were detected by Western blotting. RESULTS: The Hyp content and the expressions of collagen type I, TGF-beta1, TbetaRI and TbetaRII in the liver tissue of rats in the untreated group increased significantly as compared with those in the normal control group, while those in SA-B-treated group decreased significantly as compared with those in the untreated group. CONCLUSION: The therapeutic mechanism of SA-B in treating hepatic fibrosis may be related to inhibiting the expressions of TGF-beta1 and its receptors.
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