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桃核承气汤对肾小球硬化大鼠的作用机制研究

The Mechanism of Tao He Cheng Qi Decotion on Glomerular Sclerosis

【作者】 赵艳明

【导师】 李冀;

【作者基本信息】 黑龙江中医药大学 , 方剂学, 2008, 博士

【摘要】 目的:研究桃核承气汤对肾小球硬化大鼠的作用机制。方法:采用Platt法建立肾小球硬化大鼠模型,4周后按血肌酐水平将造模大鼠分为模型组、桃核承气汤高、低剂量组和蒙诺组,相应药物灌胃,观察各组大鼠一般状态,记录体重变化,并分别在第2、第4、第6、第8和第10周测定24小时尿蛋白定量、血尿素氮(BUN)、血肌酐(Scr),给药第10周处死大鼠,测定各组大鼠血脂、血清超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)和血液流变学情况;肾组织匀浆测SOD、MDA、谷胱甘肽过氧化物酶(GSH—PX),NO及一氧化氮合酶(NOS)。肾组织常规固定后,光镜下观察病理变化,计算肾小球硬化指数,免疫组化法检测转化生长因子β和Ⅲ型胶原。结果:模型组大鼠24小时尿蛋白定量、BUN、Scr、TC、TG、LDL、MDA、iNOS、TGF—β及C—Ⅲ均较正常组明显升高(p<0.01或p<0.05),HDL、SOD、GSH-Px、cNOS则明显降低(p<0.01或p<0.05);桃核承气汤组和蒙诺组的上述指标均有不同程度的改善(p<0.01或p<0.05)。结论:桃核承气汤能明显降低肾小球硬化大鼠的血肌酐和尿素氮,改善其肾功能和一般状态;影响肾小球硬化形成过程中细胞外基质过度沉积这一关键病理机制;减少细胞外基质主要成分Ⅲ型胶原的含量,其延缓肾小球硬化进展的具体机制包括抑制促肾小球硬化的关键细胞因子(转化生长因子β)表达、降低肾小球硬化大鼠24小时尿蛋白定量、改善其脂质代谢紊乱、氧化—抗氧化系统、影响血管活性物质、改善肾小球硬化大鼠血液流变学等方面。

【Abstract】 Objective: to study the the mechanism of TaoHeChengQi Decotion on glomerular sclerosisMethods:to establish the rat model of glomerular sclerosiswith 5/6 nephrectomy, 4 weeks later, the model group rats were randomly divided into 4 groups:pathologic group, Taohechengqi decotion low and high dose group, fosinoprili grope. After Taohechengqi decotion and fosinoprili was orally administered, each group’s blood uria nitrogen(BUN), serum creatinine (Scr), 24h urinary protein were determined in 2, 4, 6, 8,10 week later, and each group’s blood lipid, superoxide dismutase(SOD), malondialdehyde(MDA), Nitric oxide(NO), hemorheology were determined in 10 week later. And we determined each group’s SOD, MDA,GSH-Px,NO,NOS, transforming growth factor(TGF)β1, and CollagenⅢof the rats’s renal tissue.Results: As compared with pathologic group, the levels of BUN、Scr、24h urinary protein、TC、TG、LDL、MDA、NO、iNOS、TGF-β1 and CollagenⅢin treatment grope were significantly decreased (p<0.05 or p<0.01) , the level of HDL、SOD、GSH-PX、cNOS was obviously increased ( p<0.05 or p<0.01) .Conclusion:The results indicates that Taohechengqi decotion canimprove renal function of CRF rats, reduce the expression of TGF—β1 and CollagenⅢin the rats’s renal tissue, decreas the glomerulosclerosis index, modificate hemorheology of model rats. the mechanism of which probably lies in the modification of oxgen-derived free radidicals and Lipid metabolism; and the reduction of 24h urinary protein.

  • 【分类号】R285.5
  • 【下载频次】154
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