期刊文献+

垂盆草总黄酮对肝纤维化大鼠肝组织TGF-β 1和Smad7表达的影响 被引量:12

Effects of Sedum Sarmentosum Total Flavonoids on the Expression of TGF-β1 and Smad 7 in Rats with Hepatic Fibrosis
下载PDF
导出
摘要 目的:观察垂盆草总黄酮(SSTF)对CCL_4诱导肝纤维化大鼠肝组织TGF-β1和Smad7蛋白及mRNA表达的影响。方法:60只雄性SD大鼠随机分为正常组、模型组,SSTF低剂量组(100 mg·kg^(-1))、SSTF中剂量组(200 mg·kg^(-1)),SSTF高剂量组(400 mg·kg^(-1))和秋水仙碱阳性药对照组,共6组,每组10只。CCl_4皮下注射诱导大鼠肝纤维化模型,同时SSTF灌胃干预,7周后处死大鼠。采用Masson染色法检测大鼠肝脏组织病理学改变,Western blotting法检测肝脏组织TGF-β1和Smad7蛋白表达实时定量RT-PCR检测肝脏组织TGF-β1和Smad7mRNA表达。结果:与模型组比较,SSTF各剂量均能显著降低CCL_4诱导的肝纤维化程度(P<0.05);中高剂量可以显著减少肝组织中TGF-β1蛋白和mRNA表达(P<0.05),并且明显增加Smad7蛋白和mRNA表达(P<0.05)。结论:SSTF可有效地逆转实验性大鼠肝纤维化,其机制可能与下调肝组织中TGF-β1蛋白和mRNA表达及增加Smad7蛋白和mRNA表达有关。 Objective: To investigate the inhibitory effects of Sedum Sarmentosum total flavonoids (SSTF) on hepatic fibrosis in- duced by CC14, and examine the effects on the expression of TGF-β1 and Smad7. Methods: Sixty male SD rats were randomly divided into the normal control group, the model group, 100, 200 and 400 mg kg-1 SSTF groups and colchicine positive control group. The experimental model of hepatic fibrosis in rats was established by the injection of CCL4. The liver histopathology was examined by Masson stain, and the protein expression and mRNA of TGF-β1 and Smad7 were assessed by RT-PCR and Western blotting. Results: Compared with the model group, every SSTF group could significantly reduce the degree of liver fibrosis induced by CCL4 (P 〈 0.05). The middle and high dose SSTF gouprs could significantly reduce the protein expression and mRNA of TGF-β1 (P 〈 0.05), and significantly increase the protein expression and mRNA of Smad 7 ( P 〈 0.05 ). Conclusion: SSTF exhibits anti-hepatic fibrosis effects in rats through down-regulating the expression of TGF-β1 and up-regulating the expression of Smad7 in fibrotic liver tissue.
出处 《中国药师》 CAS 2015年第12期2021-2024,共4页 China Pharmacist
基金 浙江省自然科学基金资助项目(编号:LQ15H290001) 浙江中医药大学科研基金资助(编号:2014ZY08)
关键词 垂盆草总黄酮 肝纤维化 转化生长因子β1 SMAD7蛋白 Sedum Sarmentosum total flavonoids Hepatic fibrosis TGF-β1 Smad 7
  • 相关文献

参考文献11

二级参考文献69

共引文献128

同被引文献162

引证文献12

二级引证文献119

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部