摘要
目的:本实验主要研究羟甲基戊二酰辅酶A(HM G-COA)还原酶抑制剂(HR I)辛伐他汀(sim vastatin)对单侧输尿管梗阻大鼠(UUO)肾间质纤维化的影响及可能机制。方法:将26只大鼠随机分为3组:假手术组:6只;UUO组:10只;sim vastating干预组:10只。结扎单侧输尿管造成梗阻性肾病模型,术后9 d处死大鼠,取梗阻侧肾做组织学检查,观察肾间质纤维化的程度,用免疫组化方法检测肾组织中结缔组织生长因子(CTGF)、α-平滑肌肌动蛋白(-αSMA)、胶原-Ⅳ(COL-Ⅳ)的水平。结果:组织学检查发现模型组出现了明显的肾小管扩张,上皮细胞萎缩,间质炎性细胞浸润,间质纤维化,而给药组肾间质纤维化程度与模型组相比有所减轻。免疫组化结果半定量分析显示给药组CTGF(0.997 8±0.115 5)、-αSMA(0.5523±0.0631)、COL-Ⅳ(1.062 9±0.054 0)的水平较模型组明显减低(P<0.05)。结论:辛伐他汀可以抑制CTGF、抑制肾小管上皮细胞的转分化、减轻细胞外基质的积聚,从而减轻间质纤维化,发挥肾保护作用。
Objective：To evaluate the effects and possible mechanism of HMG-COA reductase inhibiter simvastatin on interstitial fibrosis of unilaterd ureteral obstruction（UUO） rats and the influence of sirnvastatin on the process. Methods： 26 rats were divided randomly into 3 groups：sham-operated 6 rats;UUO groups 10 rats ;simvastatin treatment group 10 rats. The tubulointer stitial fibrosis model was established by unilatered ureteral obstruction. These rats were sacrificed at 9 days after UUO or sham-surgery. The morphological changes was obsvered. The expression of CTGF,α- SMA,COL-IV in the obstructed kidney was assessed by imrnunchistachemistry methods. Results ：There were the obvious tubulo dilatation and epidermis cell atrophy and infiltration of the renal parenchyma with macrophages/monocytes and tubulointerstitial fibrosis in UUO groups. These changes were remarkably lighten in simvastatin treatment group. In comparison with the model group, the levels of CTGF （0.997 8±0.115 5）,α SMA（0.552 3±0.063 1）,COL-Ⅳ （1. 062 9±0. 054 0）were significantly reduced by simvastatin treatment （P〈0. 01 ）. Conclusion： Simvastatin may suppress interstitial fibrosis by effect CTGF,suppress cell proliferation,redue extracellular matrix accumulation.
出处
《中国误诊学杂志》
CAS
2006年第22期4315-4318,共4页
Chinese Journal of Misdiagnostics
