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目的 :探讨依那普利延缓肾小球硬化的有效性。方法 :运用免疫组化方法观察依那普利对 5 / 6肾切除大鼠残肾模型早、中期细胞外基质 (ECM)蓄积及其部分调控机制的影响。结果 :残肾模型术后 1周开始给予依那普利 ,术后 5周大鼠尿蛋白显著降低〔(2 .0 1± 0 .13) g/ 2 4h比 (3.10± 0 .17) g/ 2 4h〕;病理结果示 ECM多种成分的蓄积显著减少 ,肾小球硬化减轻 (硬化指数 SI为 1.6 7± 0 .76比 2 .0 0± 0 .75 ,P<0 .0 5 )。肾小球内细胞数〔(72 .2 8± 13.70 )个 /肾小球横截面比 (81.16± 16 .6 2 )个 /肾小球横截面〕及增殖细胞核抗原 (PCNA)阳性细胞数〔(6 .76± 2 .72 )个 /肾小球横截面比 (8.16± 2 .78)个 /肾小球横截面〕均显著减少 (P均 <0 .0 1)。结论 :依那普利能延缓肾小球硬化 ,减少残肾 ECM蓄积可能是其作用机制之一。
Objective: To investigate the efficacy of enalapril to delay glomerulosclerosis. Methods: The effect of enalapril on early and mid-term ECM accumulation and its regulatory mechanism in remnant kidney model of 5/6 nephrectomized rats was observed by immunohistochemistry. Results: Enalapril was given to the remnant kidney model one week after operation, and urinary protein was significantly decreased at 5 weeks after operation ([(2 .0 ± 0.13) g / 2 4h vs (3.10 ± 0.17) g / 2 4h〕; pathological results showed a significant decrease in the accumulation of ECM multiple components, glomerular sclerosis reduced (sclerotic index SI 1.6 7 ± 0.76 than 2.000 ± 0.75, P <0.05) . (72.28 ± 13.70) / glomerular cross-sectional area (81.16 ± 16.62) / glomerular cross-section and the number of proliferating cell nuclear antigen (PCNA) positive cells 〔 (6. 76 ± 2. 72) / glomerular cross section ratio (8.16 ± 2.78) / glomerular cross section] were significantly decreased (all P <0.01). Conclusion: Enalapril can delay glomerulosclerosis and reduce residual ECM accumulation may be one of its mechanisms.