摘要
目的观察缺血再灌注对肾细胞氧化损伤和细胞凋亡的影响,探讨二者在再灌注肾损伤发生机制中的作用。方法30只Wistar大鼠,分组建立急性缺血再灌注肾损伤模型,应用流式细胞术检测肾细胞凋亡率,同时测定谷胱甘肽过氧化物酶(GSH-Px)活性、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果缺血再灌注1h、2h、24h肾细胞凋亡率分别为9.58%、9.79%和11.23%,与对照组(1.51%)相比差异显著(P<0.05);各实验组SOD活力水平降低,与对照组相比差异显著(P<0.05、P<0.01),MDA生成高于对照组(P<0.05),GSH-Px在再灌注早期活力减弱,明显低于对照组(P<0.01),晚期活力基本恢复;肾细胞凋亡率与SOD活力呈负相关,与MDA生成水平正相关。结论缺血再灌注可造成肾组织氧化损伤和细胞凋亡率增高,二者协同作用参与再灌注肾病理损伤机制并可能是肾功能障碍的重要原因。
Objective To investigate the influence of ischemia-reperfusion on the oxidative damage and apoptosis of renal cell, meanwhile to value the role of oxidative damage and apoptosis in the development of reperfusion renal injury. Methods 30 Wistar rats divided into 6 groups by random and construct the acute ischemia-reperfusion renal injury model, detect the apoptosis rate by flow cytometry, and measure the GSH-Px and SOD's activity, MDA's contents. Results After ischemia-reperfusion 1 h, 2 h, and 24 h, the apoptosis rate is 9.58%, 9.79% and 11.23%, respectively, there are significantly difference between control group and experimental group (P 〈 0.05). The activity of SOD and the generation of MDA are significant different between control group and experimental group (P 〈 0.05), the generation of MDA is increased in the nonage of ischemia-reperfusion and the GSH's activity significantly decreased. At the late stage the activity recovers. The apoptosis rate of renal cell show negative correlation with SOD's activity, and positive correlation with MDA. Conclusion Ischemia-reperfusion can result in the increase of oxidative damage and apoptosis rate. The joint action of oxidative damage and apoptosis play important role in the development of reperfusion renal injury, and maybe make great contribution to renal disfunction.
出处
《深圳中西医结合杂志》
2006年第2期68-71,共4页
Shenzhen Journal of Integrated Traditional Chinese and Western Medicine
关键词
缺血再灌注
肾组织
氧化损伤
细胞凋亡
Ischemia-reperfusion
Renal tissue
Oxidative damage
Apoptosis