摘要
目的:观察糖肾平胶囊对高糖环境下脂多糖(lipopolysaccharide,LPS)刺激足细胞转化生长因子-β1(trans-forming growth factor-β1,TGF-β1)/Smad7信号转导通路的影响,并探讨其作用机制。方法:以高糖、LPS刺激足细胞建立模型,分为正常组、高糖组、高糖+LPS组、厄贝沙坦组、糖肾平小、中、大剂量组和抑制剂组。采用Western-Blotting方法检测足细胞中TGF-β1、Smad7、核因子-κB(nuclear factor-kappaB,NF-κB)的表达。结果:与正常组比,高糖组和高糖+LPS组足细胞TGF-β1、NF-κB表达明显升高(P<0.01),Smad7表达明显降低(P<0.01);抑制剂组足细胞TGF-β1、NF-κB蛋白表达比高糖组和高糖+LPS组均明显降低(P<0.01),Smad7蛋白表达明显升高(P<0.01),厄贝沙坦组TGF-β1蛋白表达比高糖组和高糖+LPS组降低(P<0.05),NF-κB蛋白表达明显降低(P<0.01),Smad7蛋白表达明显升高(P<0.01),糖肾平胶囊大、中、小剂量组足细胞中TGF-β1蛋白表达比高糖组和高糖+LPS组均降低(P<0.05),大剂量组足细胞NF-κB蛋白表达比高糖组和高糖+LPS组均明显降低(P<0.01),中、小剂量组足细胞NF-κB蛋白表达比高糖组和高糖+LPS组均降低(P<0.05),糖肾平胶囊大、小剂量组Smad7蛋白表达比高糖组和高糖+LPS组均明显升高(P<0.01)。结论:糖肾平能够降低足细胞TGF-β1、NF-κB蛋白的表达,增加Smad7蛋白表达,通过干预TGF-β1-smad7-NF-κB信号转导通路减少糖尿病肾病足细胞凋亡,可能是其防治糖尿病肾病的作用机制之一。
Objective：To observe the influence of the capsule of Tang shen ping on LPS - induced TGF - β1/Smad7 signal transduetion of podocytes under high glucose conditions, and explore its possible mechanism. Methods： Build the growth model of podoeyte induced by LPS in high glucose conditions, and divide them into 8 groups： control group;high glucose group;high glucose plus LPS group; Irbesartan group ;low - dose group of Tangshenping capsule; moderate dose group of Tangshenping capsule; high - dose group of Tangshenping capsule; inhibitor group. Detect podocyte TGF - β1, Smad7, and NF - KB protein expression of each group by Western -blotting the molecular biology level. Resldts：Compared with the control group, the expression of podocyte TGF- β1 ,NF - KB protein increased definitely （ P 〈 0.01 ）, Smad7 protein decreased definitely （ P 〈 0. 01 ） in the high glucose group and high glucose plus LPS groups. In the inhibitor group podocyte TGF - 131, NF - KB protein expression were significantly lower （ P 〈 0. 01 ）, while Smad7 protein expression was significantly higher （P 〈 0. 01 ） than the high glucose group and high glucose plus LPS groups. Compared with the high glucose group and high glucose plus LPS groups, the expression of podocyte TGF - βt decreased （ P 〈 0. 05 ）, NF - KB protein decreased definitely （ P 〈 0. 01 ）, and Smad7 protein increased definitely （ P 〈 0. 01 ） in the Irbesartan group; In the high, moderate, and low dose groups of Tangshenping capsule, podocyte TGF- 131 protein expression decreased （P 〈 O. 05 ） ; podocyte NF - KB protein expression decreased definitely （ P 〈 0. 01 ） in the high - dose group and decreased （ P 〈 0.05 ） in both moderate and low -dose groups of Tangshenping capsule; Smad7 protein increase definitely （P 〈0. 01 ） in the high and low dose groups of Tangshenping eapsule. Conclusion：Tangshenping capsule can reduce podocyte TGF- β1 ,NF- KB protein expression and increase Smad7 protein expression, reducing podoeyte apoptosis by intervention of TGF - β1 - smad7 - NF - kB signaling pathways. This mechanism may be considered as a means of prevention and treatment for diabetic nephropathy.
出处
《中国中西医结合肾病杂志》
2013年第2期107-110,共4页
Chinese Journal of Integrated Traditional and Western Nephrology
基金
国家自然基金资助项目(No.30973831)
北京市中医管理局"51510"基金资助项目(No.JJ2007-006)
