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肾上皮细胞损伤可促进肾结石形成.本文采用过氧化氢(H2O2)对人类肾小管上皮细胞(HKC)进行了氧化损伤,采用扫描电子显微镜(SEM)、X射线衍射分析(XRD)和倒置显微镜观察了HKC损伤前后的形态变化及其调控草酸钙(CaOxa)晶体成核、生长的差异;采用zeta电位分析仪检测了损伤前后HKC表面的zeta电位变化.结果表明,H2O2能明显地损伤HKC,降低细胞活性,且在H2O2浓度范围0.1～0.5mmol/L、作用时间0.5～1.5h内具有明显的剂量和时间的依赖性;使用0.5mmol/LH2O2作用1.5h可使HKC损伤达到饱和状态.HKC损伤程度增加后,其诱导的晶体数量显著增加,但晶体尺寸增加不明显(P>0.05),表明损伤细胞诱导尿石症形成主要是增加晶体的成核位点而非促进晶体的生长.本文所建立的HKC氧化损伤的模型有助于进一步阐明CaOxa结石形成的细胞机制.
Renal epithelial cell injury can promote the formation of kidney stones.In this paper, oxidative damage of human renal tubular epithelial cells (HKC) was induced by hydrogen peroxide (H2O2). The morphological changes of human renal tubular epithelial cells (HKC) were analyzed by scanning electron microscopy (SEM), X-ray diffraction (XRD) The morphological changes of HKC before and after injury and the difference of nucleation and growth of calcium oxalate (CaOxa) crystals were observed.The zeta potential changes of HKC before and after injury were detected by zeta potential analyzer.The results showed that H2O2 could obviously damage HKC, Reduce the cell activity, and in a concentration of 0.1 ~ 0.5mmol / L H2O2, the role of time within 0.5 ~ 1.5h obvious dose and time dependent; use 0.5mmol / LH2O2 1.5h can make HKC damage saturation .HKC The number of induced crystals increased significantly, but the crystal size did not increase obviously (P> 0.05), indicating that injury induced osteoclast formation mainly increases the nucleation sites rather than the crystal growth. The established model of HKC oxidative damage helps to further elucidate the cellular mechanism of CaOxa stone formation.