The protective effect of ischemic postconditioning on sinusoidal endothelial cell injury during hepatic ischemia-reperfusion.
Sun Quan
Abstract
Sun Quan
Abstract
Objective To investigate the protective effect of ischemic postconditioning(IPo) on sinusoidal endothelial cell injury during hepatic ischemia-reperfusion. Methods 24 male Wistar rats were randomly divided into 3 groups: sham-operated group, ischemia-reperfusion group (IR) and IPo group. IPo was established by several brief reperfusion-ischemia before contineous reperfusion. The activity of plasma enzyme and hyaluronic acid (HA) and the concentrations of malondialdehyde (MDA), superoxide dismute (SOD), endothelin-1 (ET-1) in hepatic tissue were determined respectively. The hepatic pathological changes were also observed. Results Compared with IR group, the activity of plasma enzyme and HA and the concentrations of MDA, ET-1 in hepatic tissue reduced markedly in IPo group (P0.01) , while the activity of SOD elevated significantly (P0.01). Sinusoidal endothelial cells were the principal target of early phase of reperfusion injury and the pathological injury in IPo group also reduced significantly. Conclusion IPo can inhibite the synthesis of oxygen free radicals and to protect the sinusoidal endothelial cells after reperfusion and has a protective effect on hepatic ischemia-reperfusion injury.
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Objective To investigate the protective effect of ischemic postconditioning(IPo) on sinusoidal endothelial cell injury during hepatic ischemia-reperfusion. Methods 24 male Wistar rats were randomly divided into 3 groups: sham-operated group, ischemia-reperfusion group (IR) and IPo group. IPo was established by several brief reperfusion-ischemia before contineous reperfusion. The activity of plasma enzyme and hyaluronic acid (HA) and the concentrations of malondialdehyde (MDA), superoxide dismute (SOD), endothelin-1 (ET-1) in hepatic tissue were determined respectively. The hepatic pathological changes were also observed. Results Compared with IR group, the activity of plasma enzyme and HA and the concentrations of MDA, ET-1 in hepatic tissue reduced markedly in IPo group (P0.01) , while the activity of SOD elevated significantly (P0.01). Sinusoidal endothelial cells were the principal target of early phase of reperfusion injury and the pathological injury in IPo group also reduced significantly. Conclusion IPo can inhibite the synthesis of oxygen free radicals and to protect the sinusoidal endothelial cells after reperfusion and has a protective effect on hepatic ischemia-reperfusion injury.
Key concepts: Reperfusion injury, Ischemia, Malondialdehyde, Medicine, Endothelin receptor, Superoxide dismutase, Endothelial stem cell, Internal medicine