Objective To investigate the effects of UCP2 in the liver ischemia- reperfusion injury. Methods Fifty male SD rats were randomized into five groups, 10 animals of each group; sham operation group (SO), 30 min ischemia group (I), 30 min ischemia-reperfusion group (I/R), 60 min I, and 60 min I/R. The expressions of ALT, ATP, UCP2 and pathological changes in the liver were observed. Results The expressions of serum ALT , UCP2 increased and ATP decreased in the liver of SO, I and IR groups by degrees. By factorial ANOVA, the changs were affected by two factors of ischemia and reperfusion synergistically. The ischemia liver was pale, and biopsy showed some scattered apoptotic cells there. The ischemia-reperfusion liver was kermesinus, and point necrosis were seen in 30 min I/R, while bridge necrosis in 60 min I/R. Conclusions UCP2 is existed in normal liver tissue. The expression of UCP2 increases and ATP decreases in ischemic liver tissue, while the changs are more significant in ischemia-reperfusion liver tissue. The over-expression of UCP2 is harmful to liver after ischemia-reperfusion injury.%目的:探讨解偶联蛋白2(UCP2)在肝缺血再灌注损伤中的作用.方法:选雄性SD大鼠50只,随机分为假手术组(SO组)、30 min缺血组(30 min I组)、30 min缺血再灌注组(30 min I/R组)、60 min缺血组(60 min I组)、60 min缺血再灌注组(60 min I/R组),每组10只.观察肝组织病理学变化,检测其ALT、ATP及UCP2的表达.结果:SO组、I组和I/R组的血清ALT和肝组织UCP2的表达依次升高,而ATP依次降低;析因方差分析显示缺血、再灌注两因素都使其升高或降低,且有协同作用.病理结果示缺血组肝组织呈灰白色,病理切片可见散在的凋亡细胞;缺血再灌注组呈暗红色,30 min I/R组病理切片可见点状坏死,而60 min I/R组可见桥接坏死.结论:UCP2在正常肝组织中已有表达;缺血后肝组织中UCP2的表达已经开始升高,ATP减少;缺血再灌注后肝组织UCP2的表达继续升高,ATP进一步减少;UCP2表达升高对肝缺血再灌注损伤有害.
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