目的 探讨在幼年肾间质微血管损伤过程中内抑素、血管内皮生长因子(VEGF)、CD31 组织定位表达的趋势、相关性及其潜在意义,以及用阿托伐他汀干预的效应.方法 采用单侧输尿管结扎(UUO)模型,将90 只SD 雄性大鼠随机分为假手术组、模型组和阿托伐他汀治疗组(治疗组).在术后第1,3,5,7,14 天每组各取6 只大鼠处死,左肾组织行Masson 染色,动态观察肾脏病理学变化,并用免疫组织化学方法测定肾组织中内抑素、VEGF、CD31 的表达变化.结果 随着梗阻时间延长UUO 模型组内抑素蛋白表达进行性增高, 而VEGF 及CD31 蛋白表达水平却逐渐下降；与UUO 模型组相比,治疗组内抑素蛋白表达减少,而VEGF 及CD31 蛋白表达增高.内抑素与VEGF 及CD31 之间呈负相关.结论 在幼年大鼠肾间质微血管损伤过程中,内抑素表达上调具有重要的致病意义,而阿托伐他汀可以通过下调内抑素减轻肾间质微血管损伤.%Objective To investigate the trend for tissue-specific expression, relevance and the potential significance of endostatin (ENS), vascular endothelial growth factor (VEGF) and CD31 during renal microvascular injury in you ng rats, and to explore the intervention effect of atorvastatin. Methods Unilateral ureteral obstruction (UUO) models were established in SD rats. A total of 90 male SD rats were randomly divided into shame operation group, UUO model group and atorvastatin-treated group. On days 1, 3, 5, 7 and 14 after operation, every 6 SD rats from each group were sacrificed for dynamic observation of kidney pathological changes with Masson staining in the left kidney tissue where altered expressions of ENS, VEGF and CD31 was determined subsequently by immunohistochemistry. Results Along with the increase of obstruction time, the UUO group showed progressively increased ENS expression but a gradual decline in expressions of VEGF and CD31. On the contrary, the atorvastatin-treated group had a decline in the expression of EN,S but an elevation in expressions of VEGF and CD31 as compared with the UUO group. The expression of ENS was negatively correlated with those of VEGF and CD31. Conclusion In the process of tubulointerstitial microvascular injtry, the up-regulated expression of ENS exhibits an important role in pathogenesis. Atorvastatin may alleviate the tubulointerstitial microvascular injury by down-regulating the expression of ENS.
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