The Role Of ERS In Apotosis Of HKC Cells Induced By Contrast Media And The Protection From Atorvastatin

[Objective] To investigate the the role of ERS in apotosis of HKC cells induced by CM and the Protection from Atorvastatin.[Methods] Under the pretreatment with atorvastatin and hypoxia-ischemic condition, As the research object,human renal tubular epithelial cell(HKC)lines were randomly divided into six groups: control, contrast group(pretreated with 120 mg I/m L lopromide for 2 hours) and anti-apoptotic group(pretreated with 10mmol/L NAC for 2 hours followed by 120 mg I/m L lopromide for 2 hours), low, medium and high dose of ATO group(pretreatment with ATO at dose of 10-8mol/L, 10-7mol/L and 10-6mol/L, respectively, and followed by 120 mg I/m L lopromide for 2 hours). Cell proliferation was detected by CCK-8 and cell injury by detection of LDH. Intracellular MPO, MDA and extracellular SOD were analyzed by automatic biochemical analyzer.[Results] CM reduced cell viability and caused damage of normal HKC cells and HKC cells under the conditions of ischemia and hypoxia. And the levels of intracellular MPO, MDA decreased, extracellular SOD increased after treated with contrast media. When pretreated with ATO followed by CM, cell viability increased, contrast-induced cell injury reduced, the levels of intracellular MPO, MDA increased, extracellular SOD decreased. Moreover, the effect of ATO on HKC cells under conditions of ischemia and hypoxia was more effective than normal HKC cells, and showed a significant dose-dependent manner.And CM significantly increased the apoptosis rate and expression of GPR78, CHOP and caspase-12. Anti-apoptotic agent significantly decreased apoptosis rate and expression of caspase-12, but for GPR78 and CHOP. Pretreatment with atorvastatin reduced the expression of GPR78, CHOP and caspase-12, and showed as significant dose-dependent.[Conclusion] Under the conditions of ischemia and hypoxia,the CM induced the injury and apoptosis of HKC cells.These results might relate to the intracellular oxidative stress and ERS. ATO has a protective effect on contrast-induced injury of HKC cells, which suggest that ATO may reduce contrast-inducedinjury of HKC cells by inhibition of intracellular oxidative stress and ERS.