论文部分内容阅读
目的:建立小鼠肾脏缺血-再灌注损伤模型,并观察褪黑素(MT)对小鼠急性肾脏缺血-再灌注损伤(IRI)的保护作用及其机制。方法:昆明种小鼠40只,随机分为假手术对照组、单纯缺血-再灌注组、缺血-再灌注+MT高、低剂量组。测定缺血-再灌注24h后小鼠肾组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活力和丙二醛(MDA)含量变化,并观察肾脏组织的病理学改变。结果:与假手术对照组相比,单纯缺血-再灌注组肾小管上皮细胞呈明显的缺血性改变,肾组织MDA含量明显增加(P<0.01),SOD、GSH-PX活力明显降低;缺血-再灌注+MT高、低剂量组与单纯缺血-再灌注组相比,肾组织MDA含量明显降低(P<0.01),SOD、GSH-PX活力明显增加,肾小管上皮细胞缺血性改变减轻。结论:MT通过抗氧化,对小鼠急性肾缺血-再灌注损伤有保护作用。
OBJECTIVE: To establish a mouse model of renal ischemia-reperfusion injury and observe the protective effect and mechanism of melatonin (MT) on acute renal ischemia-reperfusion injury (IRI) in mice. Methods: Forty Kunming mice were randomly divided into four groups: sham operation control group, ischemia / reperfusion group, ischemia / reperfusion + MT high and low dose groups. The changes of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) activity and malondialdehyde (MDA) content in kidney homogenate of mice were measured 24h after ischemia-reperfusion, Pathological changes of the tissue. Results: Compared with the sham operation group, the renal tubular epithelial cells in ischemia - reperfusion group showed obvious ischemic changes, the content of MDA in renal tissue increased significantly (P <0.01) and the activities of SOD and GSH - PX decreased obviously. Compared with the ischemia-reperfusion group, the MDA content in the ischemia-reperfusion + MT high and low dose groups was significantly decreased (P <0.01), the activities of SOD and GSH-PX were significantly increased, the renal tubular epithelial cells Change of sexual lessen. Conclusion: MT can protect mice from acute renal ischemia-reperfusion injury through antioxidation.