Effect of ischemic postconditioning on renal injury induced by intestinal ischemia-reperfusion and expression of Nrf2 in mice / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effect of ischemic postconditioning (IPO) on renal injury induced by intestinal ischemia-reperfusion (I/R) and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in mice.Methods Thirty-six healthy male C57BL/6J mice,aged 9-12 weeks,were randomly divided into 3 groups ( n =12 each)sham operation group ( S group),I/R group,and IPO + I/R group ( group IPO).Intestinal I/R was produced by occlusion of superior mesenteric artery for 45 min followed by 2 h reperfusion.The mice underwent 3 cycles of 30 s reperfusion and 30 s ischemia at the end of 45 min ischemia before 2 h reperfusion.Blood samples were collected from carotid artery at 2 h of reperfusion and then the mice were sacrificed.The kidney was removed for microscopic examination.The pathological changes of the kidney were scored.The concentrations of serum blood urea nitrogen (BUN),creatinine (Cr) and neutrophil gelatinase-associated lipocalin (NGAL)were detected.The expression of Nrf2 and heme oxygenase- 1 ( HO- 1 ),superoxide dismutase (SOD) activity,and the content of malondialdehyde (MDA),TNF-α,IL-6 and IL-10 were determined in renal tissues.Results The concentrations of serum BUN,Cr and NGAL,MDA content and the expression of Nrf2 and HO- 1 were significantly higher,SOD activity was significantly lower,and the pathological score was significantly higher in group I/R that in group S ( P ＜ 0.05).The concentrations of serum BUN,Cr and NGAL and MDA content were significantly lower,the expression of Nrf2 and HO-1 and SOD activity were significantly higher,and the pathological score was significantly lower in group IPO that in group I/R ( P ＜0.05).There was no significant difference in the content of TNF-αα,IL-6 and IL-10 among all groups(P＞0.05).Conclusion IPO can alleviate the renal injury induced by intestinal I/R through promoting the expression of Nrf2 and up-regulating the expression of HO-1 in mice.