摘要

An oxidative injury model of human kidney proximal tubule epithelial cell line (HKC) was used to investigate the difference of crystallization of calcium oxalate (CaOxa) modulated by HKC before and after injury. Cell viability was examined by using Cell Counting Kit (CCK-8) assay; the change of expression of crystal adherent molecule osteopontin (OPN) on HKC after injury was observed by laser confocal microscope; the morphological change of HKC was observed by inverted microscope; the microstructure of HKC and the crystals induced by HKC were observed by means of scanning electron microscopy (SEM); the crystal component was characterized by X-ray diffraction (XRD). Calcium oxalate dihydrate (COD) crystals were mainly induced from CaOxa supersaturated solution by normal -HKC, while COD crystals and calcium oxalate monohydrate (COM) crystals were simultaneously induced by injured HKC. The endocytosis of normal HKC to COD crystals was strong, but weak for injured HKC. After expression of OPN, the injured HKC can promote nucleation and aggregation of CaOxa crystals. It increases the risk of urolithiasis formation.