摘要
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 urolithiasis. In this study,hydrogen peroxide （H2O2） was used to induce oxidative cellular injury of human renal tubular epithelial cells （HKC）. The morphological changes of HKC cells after oxidative injury were investigated. The difference on the regulation of nucleation and growth of calcium oxalate （CaOxa） crystals by HKC cells before and after injured were also investigated by means of scanning electronic microscopy （SEM）,X-ray diffraction （XRD） and inverted microscopy. The change of zeta potential on cells before and after injured was determined by a zeta potential analyzer. It was indicated that H2O2 could significantly injure HKC cells,and decrease the cell viability in dose-dependent and time-dependent manner in the concentrations range from 0.1 to 0.5 mmol/L and in the exposure time from 0.5 to 1.5 h. The maximal damage was appeared at the point of 0.5 mmol/L H2O2 for 1.5 h. The increased damage level of HKC cells could significantly increase the quantity of CaOxa crystals,but could hardly increase the size of crystals （P 〉0.05）. It suggested that the formation of stones induced by injured HKC cells was probably by providing the nucleating sites for crystals,but not by promoting crystal growth. The in vitro oxidative damage model of HKC established in this paper is helpful for further clarifying the cellular mechanisms of CaOxa stone formation.
出处
《中国科学：化学》
CAS
CSCD
北大核心
2010年第8期1186-1192,共7页
SCIENTIA SINICA Chimica
基金
国家自然科学基金(20971057)的资助
关键词
草酸钙
生物矿化
细胞调控
肾结石
肾小管上皮细胞
calcium oxalate
biomineralization
cell modulation
urolithiasis
renal tubular epithelial cell
