川芎嗪抗肾缺血再灌注损伤脂质过氧化作用的机制研究

Interfering effect of ligustrazine on lipid peroxidation during renal ischemia-reperfusion injury in rabbits

目的:观测兔肾缺血再灌注损伤时脂质过氧化的变化、探讨中药川芎嗪的干预作用及机制。方法:日本大耳白兔30只,随机均分为对照组、再灌注组和川芎嗪组。复制在体兔肾缺血再灌注损伤动物模型,在缺血前、缺血1h、再灌注5h分别经颈总动脉抽血检测黄嘌吟氧化酶(XO)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;实验结束时取肾组织检测XO、SOD活性及MDA含量,观察超微结构变化,作对比分析。结果:川芎嗪组血浆XO活性和MDA含量显著低于再灌注组(均P<0.01);SOD活性高于再灌注组(P<0.05)。川芎嗪组与再灌注组相比,肾组织的XO活性、MDA含量明显降低,SOD活性明显升高,差异非常显著(均P<0.01)。再灌注组肾小球毛细血管内皮细胞,脏层上皮细胞超微结构严重损害,川芎嗪组大部分肾组织上述部位存在不同程度损伤性改变,但比再灌注组明显减轻。结论:川芎嗪可通过减少氧自由基的生成,增强氧自由基的清除,抑制脂质过氧化反应,有效减轻肾缺血再灌注损伤。

Objective To observe the change of lipid peroxidation during renal isehemia- reperfusion injury, and to investigate the effect of ligustrazine on it. Methods 30 rabbits were divided into 3 groups randomly （each n = 10） ： control group, ischemia-reperfusion group （IR group）, and ligustrazine group （LZ group）. The blood was gathered from common carotid artery at pre-ischemia, ischemia 1h, reperfusion 5 h to detect the activity of xanthine oxidase （XO） and superoxide dismutase （SOD）, and the content of malondialdehyde （MDA）. The renal tissue was collected at the end of experiment to detect the activity of XO and SOD and the Content of MDA, and to observe the uhrastructural changes with electronic microscope. Resudts The activity of XO and the content of MDA in plasma and renal tissue were significant lower, while the activity of SOD in plasma and renal tissue were significant higher in LZ group than those in IR group （P 〈 0.01 or P 〈 0.05）. There were serious uhrastructural changes in glomerular capillary endothelium and podocyte/capsule epithelium in IR group, but were alleviated in LZ group. Conclusion Ligustrazine may decrease the generation and enhance the clearance of oxygen free radical, and restrain lipid peroxidation, and finally attenuate renal isehemiareperfusion injury.