Propofol Prevents Renal Ischemia-Reperfusion Injury via Inhibiting the Oxidative Stress Pathways

作者：Yingjie Li, Dandan Zhong, Lei Lei, Yingli Jia, Hong Zhou, Baoxue Yang · 发表于：Cellular Physiology and Biochemistry · 年份：2015 · DOI：10.1159/000430329 · 被引用次数：73 · 研究领域：Cardiac Ischemia and Reperfusion、Acute Kidney Injury Research、Cell death mechanisms and regulation

BACKGROUND/AIMS: Renal ischemia/reperfusion injury (IRI) is a risk for acute renal failure and delayed graft function in renal transplantation and cardiac surgery. The purpose of this study is to determine whether propofol could attenuate renal IRI and explore related mechanism. METHODS: Male rat right kidney was removed, left kidney was subjected to IRI. Propofol was intravenously injected into rats before ischemia. The kidney morphology and renal function were analyzed. The expression of Bax, Bcl-2, caspase-3, cl-caspase-3, GRP78, CHOP and caspase-12 were detected by Western blot analysis. RESULTS: IR rats with propofol pretreatment had better renal function and less tubular apoptosis than untreated IR rats. Propofol pretreated IR rats had lower Bax/Bcl-2 ratio and less cleaved caspase-3. The protein expression levels of GRP78, CHOP and caspase-12 decreased significantly in propofol pretreated IR rats. In vitro cell model showed that propofol significantly increased the viability of NRK-52E cells that were subjected to hypoxia/reoxygenation (H/R) in a dose-dependent manner. The effect of propofol on the expression regulation of Bax, Bcl-2, caspase-3, GRP78, CHOP was consistent in both in vitro and in vivo models. CONCLUSION: Experimental results suggest that propofol prevents renal IRI via inhibiting oxidative stress.