【摘要】 目的建立小鼠肾脏缺血-再灌注损伤模型,观察褪黑素对热休克蛋白合成的影响,了解褪黑素对小鼠急性肾脏缺血-再灌注损伤的保护作用及其机制。方法昆明种小鼠40只,随机分成假手术组、缺血-再灌注组和褪黑素高、低剂量组。缺血-再灌注24 h后观察肾脏组织的病理学改变,并通过免疫组织化学方法观察小鼠肾脏热休克蛋白的表达。结果与假手术组相比,缺血-再灌注组肾小管上皮细胞呈明显的缺血性改变,肾小球内中性粒细胞数目明显增多,肾脏热休克蛋白表达明显增强;褪黑素高、低剂量组与缺血-再灌注组相比,肾小管上皮细胞缺血性改变减轻,肾小球内中性粒细胞数目明显减少,肾脏热休克蛋白表达明显增强。结论褪黑素通过诱导热休克蛋白的合成,能减轻小鼠急性肾缺血-再灌注的损伤。更多还原

【Abstract】 Objective For setting up a mice model of renal ischemia-reperfusion injury(IRI),and to investigate the effects of melatonin(MT) on heat shock protein 70(HSP70) expression in mice and to discuss its protection mechanisms.Methods A model of renal ischemia-reperfusion injury was set up.Forty mice were randomly divided into sham operated group,IRI group,and IRI+MT(1 mg,10 mg) group.The renal pathologic changes were observed.The HSP70 expression in kidney was evaluated by immunohistochemistry.Results As compared with those of sham operated group,some ischemic changes in the renal tubular epithelical cells was observed,neutrophils in glomerular and the HSP70 expression increased significantly in IRI group.As compared with those of IRI group,some mild ischemic changes in the renal tubular epithelical cells was observed,neutrophils in glomerular decreased and the HSP70 expression increased significantly in IRI+MT group.Conclusion The results indicated that the administration of MT could increase HSP70 expression and alleviate renal ischemia-reperfusion injury in mice.更多还原