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采用H2O2对非洲绿猴肾上皮细胞(Vero)进行了损伤,通过检测细胞存活率、培养基中超氧化物歧化酶(SOD)浓度、丙二醛(MDA)释放量和细胞表面晶体粘附分子骨桥蛋白(OPN)的表达量变化,检测了细胞的损伤程度.H2O2对Vero细胞的损伤作用呈现时间依赖性和浓度依赖性;细胞损伤后,MDA释放量增加,SOD浓度降低,OPN表达量显著增加,导致粘附的晶体量增加.利用扫描电子显微镜(SEM)和X射线衍射(XRD)研究了细胞损伤前后对草酸钙(CaOxa)晶体生长的调控作用.对照组细胞诱导生成的CaOxa晶体棱角圆钝,同时含有一水草酸钙(COM)和二水草酸钙(COD)晶体;而损伤细胞诱导生成的晶体形状不规则,棱角尖锐,主要为COM晶体,因此,细胞损伤后增加了草酸钙结石形成的危险性.所建立的Vero细胞氧化损伤模型有助于从细胞水平上阐明草酸钙结石的形成机制.
H2O2 was used to injure the Vero cells in vitro. The cell viability, the concentration of superoxide dismutase (SOD), the release of malondialdehyde (MDA) and the crystal adhesion molecule bone The expression of OPN was detected to detect the degree of cell injury.H2O2 had a time-dependent and concentration-dependent manner on the injury of Vero cells.After cell injury, the release of MDA increased, the concentration of SOD decreased and the expression of OPN was significant Increased the amount of crystals which led to the adhesion.Calcium oxalate (CaOxa) crystal growth was examined by scanning electron microscopy (SEM) and X-ray diffraction (XRD) before and after cell injury.The control group cells induced CaOxa crystal edge Round and dull, containing both calcium oxalate monohydrate (COM) and calcium oxalate dihydrate (COD) crystals. However, the crystals induced by damaged cells are irregular in shape and angular in shape, mainly COM crystals. Therefore, calcium oxalate The risk of stone formation.The Vero cell oxidative damage model established can help to clarify the formation mechanism of calcium oxalate stones at the cellular level.