Valsartan protects HK‐2 cells from contrast media‐induced apoptosis by inhibiting endoplasmic reticulum stress

• DOI: 10.1002/cbin.10521
• Publication Date: 2015-08-06T14:18:44Z
• Authors: Ping‐an Peng; Le Wang; Qian Ma; Yi Xin; Ou Zhang; Hong‐ya Han; Xiao‐li Liu; Qing‐wei Ji; Yu‐jie Zhou; Ying‐xin Zhao
• Keywords: 0301 basic medicine; 0303 health sciences; Dose-Response Relationship, Drug; Cell Survival; Contrast Media; Apoptosis; Endoplasmic Reticulum Stress; Protective Agents; 3. Good health; Mice; 03 medical and health sciences; Kidney Tubules; 13. Climate action; Animals; Humans; Valsartan; Endoplasmic Reticulum Chaperone BiP

Contrast-induced acute kidney injury (CI-AKI) is associated with increasing in-hospital and long-term adverse clinical outcomes in high-risk patients undergoing percutaneous coronary intervention (PCI). Contrast media (CM)-induced renal tubular cell apoptosis reported to participate this process by activating endoplasmic reticulum (ER) stress. An angiotensin II type 1 receptor (AT1R) antagonist can alleviate ER stress-induced streptozotocin (STZ)-induced diabetic mice reduce CM-induced reducing oxidative stress reversing the enhancement of bax mRNA reduction bcl-2 mRNA, but effect AT1R blocker on pathogenesis CI-AKI still unknown. In study, we explored valsartan meglumine diatrizoate-induced human measuring changes stress-related biomarkers. The results showed that diatrizoate caused significant up-regulating expression markers, including glucose-regulated protein 78 (GRP78), transcription factor 4 (ATF4), CCAAT/enhancer-binding protein-homologous (CHOP) caspase 12, a time- dose-dependent manner, which could be alleviated preincubation valsartan. conclusion, had potential nephroprotective inhibiting