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目的研究扶肾降浊方对系膜增生性肾小球肾炎(MsPGN)大鼠肾小管间质损害的疗效机制。方法在MsPGN动物模型基础上,延长建模时间至20周,使其自然发展为肾小管间质损害模型。实验设中药组、西药组、模型组及空白组。中药组给予扶肾降浊方17.01g·kg-1灌服,西药组以贝那普利1.8mg·kg-1灌服,模型组和空白组给予等量生理盐水,连续20周,分别于实验第12,16和20周末剖取大鼠肾组织,采用实时荧光定量-聚合酶链式反应(RT-PCR)检测大鼠肾组织转化生长因子-β1(TGF-β1)、Smad3、Smad7及整合素连接激酶(ILK) mRNA表达水平。结果模型大鼠肾组织TGF-β1/Smads/ILK信号转导通路发生改变,其中TGF-β1、Smad3、ILK mRNA表达上调,Smad7 mRNA表达下调。扶肾降浊方随着给药周期的延长能部分逆转肾小管损害造成的上述mRNA表达异常。结论扶肾降浊方对MsPGN大鼠肾小管间质损害保护作用机制可能与调节TGF-β1/Smads/ILK信号转导通路有关。
Objective To study the therapeutic mechanism of Fu Shen Jiang Zhuo Fang on tubulointerstitial damage in rats with mesangial proliferative glomerulonephritis (MsPGN). Methods Based on the MsPGN animal model, the modeling time was extended to 20 weeks, making it a natural model of tubulointerstitial damage. Experimental set Chinese medicine group, western medicine group, model group and blank group. The Chinese medicine group was administered with 17.01g · kg-1 of Fufang Jiangzhuo Decoction, while the western medicine group was fed with benazepril 1.8mg · kg-1. The rats in the model group and the blank group were given the same amount of normal saline for 20 weeks, Rat renal tissues were harvested at the end of the twelfth, sixteenth, and seventy weeks. The expression of TGF-β1 (TGF-β1), Smad3, Smad7 and TGF-β1 in rat renal tissues were detected by real-time fluorescence quantitative polymerase chain reaction Integrin Ligase (ILK) mRNA expression levels. Results The TGF-β1 / Smads / ILK signal transduction pathways were changed in the model rats. TGF-β1, Smad3 and ILK mRNA were up-regulated and Smad7 mRNA was down-regulated. Fuzhengjiangzhuo prescription with the extension of the dosing period can partially reverse the renal tubular damage caused by the above mRNA abnormalities. Conclusion The protective mechanism of Fu Shen Jiang Zhuo Fang on tubulointerstitial damage in MsPGN rats may be related to the regulation of TGF-β1 / Smads / ILK signal transduction pathway.