丹参酮ⅡA干预肝纤维化模型大鼠相关信号通路相关因子的表达

被引:29
作者
张彩华
李骢
李华军
郭连英
贾玉杰
机构
[1] 大连医科大学病理生理学教研室
关键词
丹参酮; 组织工程; 转化生长因子β; 骨形态发生蛋白7; 模型,动物; 实验动物; 消化系统损伤动物模型; 肝纤维化; 丹参酮ⅡA; 四氯化碳; Smad; 信号通路; 辽宁省自然科学基金;
D O I
暂无
中图分类号
R285.5 [中药实验药理]; R-332 [医用实验动物学];
学科分类号
100402 [劳动卫生与环境卫生学]; 100806 [中药药理学];
摘要
背景:肝纤维化是一种由多种病因导致的以细胞外基质过度沉积为特点的慢性活动性疾病,目前中药治疗肝纤维化具有显著优势。研究表明丹参治疗肝纤维化具有较好的疗效,但其作用机制尚需进一步研究。目的:研究丹参酮ⅡA对肝纤维化大鼠肝脏转化生长因子β-Smads信号通路相关因子转化生长因子β,骨形态发生蛋白7及Smad6,7基因表达的影响。方法:随机将SD大鼠分为正常对照组、模型组和丹参酮ⅡA治疗组,模型组和丹参酮ⅡA治疗组给予橄榄油稀释的体积分数10%四氯化碳5 m L/kg皮下注射,每周2次,共8周,建立肝纤维化模型。建模后第4周,丹参酮ⅡA治疗组给予丹参酮ⅡA治疗至第8周。正常对照组以同样方法皮下注射橄榄油。结果与结论:Western印迹检测和RT-PCR检测显示,与正常对照组相比,模型组大鼠肝组织转化生长因子β的表达明显增加(P<0.01),而其抑制因子骨形态发生蛋白7和Smad6,7的表达明显减少(P<0.01),丹参酮ⅡA可明显逆转上述因子的表达(P<0.01)。结果提示,丹参酮ⅡA治疗肝纤维化可能与其抑制转化生长因子β,增加其抑制因子骨形态发生蛋白7和Smad6,7的表达有关。
引用
收藏
页码:4345 / 4350
页数:6
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