肾草酸钙结石大鼠肾小管细胞损伤的机制

目的探讨肾草酸钙结石大鼠肾小管上皮细胞损伤的机制,为临床预防和治疗肾结石提供理论依据。方法 20只大鼠随机分为模型组和对照组,每组10只。模型组制备肾草酸钙结石大鼠模型。分离大鼠肾小管上皮细胞并进行培养,用乳酸脱氢酶释放法检测上皮细胞活性,酶联免疫吸附法检测肾小管上皮细胞中caspase-3活性,Western blot方法检测肾小管上皮细胞中Bcl-2、Bax和Cyto C的表达。结果模型组大鼠肾小管上皮细胞活性显著低于对照组(P<0.05),且细胞中caspase-3活性显著升高(P<0.05)。与对照组比较,模型组Bcl-2蛋白表达显著降低(P<0.05),Bax蛋白表达显著升高(P<0.05),Cyto C释放显著增多(P<0.05)。结论肾草酸钙结石大鼠肾小管上皮细胞的损伤可能是由线粒体途径介导的细胞凋亡引起的。

Mechanism of renal tubular cell injury in rats with renal calcium oxalate calculus

Objective To investigate the mechanism of renal tubular epithelial cell injury in rats with renal calcium oxalate calculus,and to provide a theoretical basis for the clinical prevention and treatment of renal calculus.Methods Twenty rats were randomly divided into model group and control group,ten rats in each group.The models of renal calcium oxalate calculus were established in model group.The renal tubular epithelial cells were isolated and cultured,then the cells activity was detected by lactate dehydrogenase release assay,the caspase-3 activity in renal tubular epithelial cell was detected by enzyme-linked immunosorbent assay,and the expressions of Bcl-2,Bax and Cyto C in renal tubular epithelial cell were detected by Western blot.Results The activity of renal tubular epithelial cells of rats in model group was significantly lower than that in control group(P<0.05),and the activity of caspase-3 in model group was significantly higher than that in control group(P<0.05).Compared with control group,the expression of Bcl-2 protein was significantly lower(P<0.05),the expression of Bax protein was significantly higher(P<0.05),and the Cyto C release increased significantly(P<0.05).Conclusion The injury of the renal epithelial cells of rats with renal calcium oxalate calculus may be caused by mitochondrial pathway mediated apoptosis.