HKC细胞损伤对草酸钙晶体成核和聚集的促进作用

Promotion on Nucleation and Aggregation of Calcium Oxalate Crystals by Injury of HKC Cell

采用H2O2对人肾小管上皮细胞(HKC)进行损伤.HKC细胞受损伤后,其活力降低,并表达骨桥蛋白(OPN).损伤细胞促进草酸钙晶体的成核、聚集,并促进一水合草酸钙(COM)晶体的形成,但对晶体生长的促进作用不明显.本文研究结果表明,HKC细胞损伤后增加了肾结石形成的危险性.

Human renal tubular epithelial cells（HKC） were injured by H2O2.Cell damage caused the decreased viability of HKC,and the increased expression of osteopontin（OPN）.With the injury time increased,cell viability continued to decline,and OPN expression also increased continuously.Compared to control cells,the number of crystals induced by the damaged cells increased significantly,and the aggregation level of the crystal also increased,but the effect on growth of calcium oxalate crystals was not significant.The control cells mainly induced formation of calcium oxalate dihydrate（COD） crystals.However,the damaged cells simultaneously induced formation of a greater amount of calcium oxalate monohydrate（COM）.This indicated that both the nucleation and aggregation of calcium oxalate crystals and the formation of COM crystals were promoted.The results suggest that damage of renal tubular epithelial cells might increase the risk of kidney stone formation.