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.
ABSTRACT
Objective To observe the effects of exogenous sodium phosphocreatine (PCr) on cerebral repeffusion injury of rats after ischemia in order to explore the potential mechanism. Method Thirty-six healthy adult male Wistar rats with body weight 200- 220 g were randomly (random number) divided into sham operation group, ischemic reperfusion (I/R) group and PCr treatment group. The I/R model was established by using electro-cauterizing bilateral vertebral arteries and occluding bilateral common carotid arteries with atraumatic carotid clasps for 10 min, and then the clasps were released for 48 hours reperfusion. In sham operation group, bilateral common carotid arteries were exposed without occlusion. In PCr treatnent group, PCr in dose of 150 mg/kg was administered intravenously 60 min before the occlusion of bilateral common carotid arteries. Normal saline was administered intravenously instead of PCr into rats of I/R group. After reporfusion for 48 hours, the rats were sacrificed and brains removed for detections of neuron apoptosis by using TUNEL, malondialdebyde (MDA) level by using chromtometry and calmodulin (CaM) activity by using ELISA. Results Compared with sham operation group, TUNEL-positive cells, MDA level and CaM activity increased in I/R group and PGr treatment group ( P ＜0.01). Compared with I/R group, TUNEL-positive cells, MDA level and CaM activity were lower significantly in PCr treatment group ( P ＜ 0.01). Conclusions PCr can lessen cerebral ischemic reperfusion injury and neuron apoptosis, the mechanism maybe relates to the attenuation of abnormalities in calcium balance and reduction of oxygen free radicals by PCr.