近端肾小管上皮细胞损伤后对草酸钙结晶的促进作用

目的 研究过氧化氢(H2O2)对人肾小管上皮细胞(HKC)的氧化损伤作用,探讨结晶时间对损伤HKC调控草酸钙(CaOxa)晶体生长的影响.方法 通过检测细胞成活率和细胞中丙二醛释放量的变化评价HKC的损伤程度;利用扫描电镜研究HKC损伤对CaOxa结晶的影响.结果 0.3 mmol/L H2O2作用HKC 1 h后,细胞活性降为79.0%,作用2 h后,细胞活性仅37.8%(P＜0.05).正常HKC形态饱满,细胞连接成片,鞭毛、突触等均完好.0.3 mmol/L H2O2作用1 h后,HKC发生明显皱缩,细胞表面粗糙,周围出现细胞碎片;作用2 h后,细胞皱缩更明显,部分细胞脱落.对照组细胞只诱导少量二水草酸钙形成,损伤细胞不仅诱导一水草酸钙(COM)形成,而且增加CaOxa晶体的数量和聚集程度;用CaOxa过饱和溶液长时间孵育对照组细胞后亦可以产生损伤.结论 H2O2能使HKC产生氧化性损伤,促进COM晶体成核和聚集;晶体在尿路中长时间滞留是肾结石形成的危险因素.

Abstract：

Objective To investigate the injury caused by hydrogen peroxide (H2O2) on human renal tubular epithelial cell (HKC) and its effect on calcium oxalate (CaOxa) crystal crystallization time before and after the injury. Methods The injury degree of HKC by H2O2 was measured by detecting the cell survival rate and the concentration change of malonaldehyde (MDA). CaOxa crystallization was investigated by scanning electron microscopy (SEM). Results Control cells induced only a small amount of calcium oxalate dihydrate (COD) crystals, while the injured cells not only induced calcium oxalate monohydrate (COM) crystals, but also increased the number and aggregation of CaOxa crystals. After incubating with CaOxa supersaturated solution, the control group HKC cells could be injured as well. Conclusions H2O2 can cause oxidative damage on HKC. The injured HKC promotes the nucleation and aggregation of COM crystals. In the body environment, the long-term presence of crystals in urinary tract is a risk factor for stone formation.

Promotion of calcium oxalate crystallization after human renal tubular epithelial cell injury

Objective To investigate the injury caused by hydrogen peroxide (H2O2) on human renal tubular epithelial cell (HKC) and its effect on calcium oxalate (CaOxa) crystal crystallization time before and after the injury. Methods The injury degree of HKC by H2O2 was measured by detecting the cell survival rate and the concentration change of malonaldehyde (MDA). CaOxa crystallization was investigated by scanning electron microscopy (SEM). Results Control cells induced only a small amount of calcium oxalate dihydrate (COD) crystals, while the injured cells not only induced calcium oxalate monohydrate (COM) crystals, but also increased the number and aggregation of CaOxa crystals. After incubating with CaOxa supersaturated solution, the control group HKC cells could be injured as well. Conclusions H2O2 can cause oxidative damage on HKC. The injured HKC promotes the nucleation and aggregation of COM crystals. In the body environment, the long-term presence of crystals in urinary tract is a risk factor for stone formation.