Protective effect of ischemic-postconditioning on hepatic ischemia-reperfusion injury in rats
Sun Shuxia
Abstract
Sun Shuxia
Abstract
Objective To investigate the protective effect of ischemic-postconditioning (IPO) on hepatic ischemia-reperfusion injury in rats. Methods 75 Sprague-Dawley rats were randomly divided into shamoperated(S),ischemia-reperfusion(IR) and IPO group to establish the model of acute liver ischemia-reperfusion injuries. Before persistent reperfusion,animals in IPO group were given six brief reperfusion-ischemia. The sample of blood and hepatic tissue of rats in all groups were taken for detections. Results Compared with in IR group,the concentrations of serum AST and ALT and malondialdehyde in hepatic tissues in IPO group decreased markedly(P0.01),while the concentrations of superoxide dismutase increased significantly(P0.01);the hepatic pathological damage also relieved obviously in IPO group. The expression levels of enos protein in IPO group were higher than that of IR group at the 7 min reperfusion. Conclusion IPO can attenuate hepatic ischemia-reperfusion injury by activating the prosurvival kinases of eNOS in accordance with the RISK pathway and reducing the concentrations of oxygen free radical.
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Objective To investigate the protective effect of ischemic-postconditioning (IPO) on hepatic ischemia-reperfusion injury in rats. Methods 75 Sprague-Dawley rats were randomly divided into shamoperated(S),ischemia-reperfusion(IR) and IPO group to establish the model of acute liver ischemia-reperfusion injuries. Before persistent reperfusion,animals in IPO group were given six brief reperfusion-ischemia. The sample of blood and hepatic tissue of rats in all groups were taken for detections. Results Compared with in IR group,the concentrations of serum AST and ALT and malondialdehyde in hepatic tissues in IPO group decreased markedly(P0.01),while the concentrations of superoxide dismutase increased significantly(P0.01);the hepatic pathological damage also relieved obviously in IPO group. The expression levels of enos protein in IPO group were higher than that of IR group at the 7 min reperfusion. Conclusion IPO can attenuate hepatic ischemia-reperfusion injury by activating the prosurvival kinases of eNOS in accordance with the RISK pathway and reducing the concentrations of oxygen free radical.
Key concepts: Medicine, Reperfusion injury, Malondialdehyde, Ischemia, Enos, Superoxide dismutase, Pathological, Anesthesia