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作 者:嵇金陵 汤钱球 张小云[1] JI Jin-ling;TANG Qian-qiu;ZHANG Xiao-yun(Department of Clinical Laboratory,the Huaian First Hospital Affiliated to Nanjing Medical University,Huaian 223300,Jiangsu,China)
机构地区:[1]南京医科大学附属淮安第一医院检验科,江苏淮安223300
出 处:《医学临床研究》2018年第8期1513-1516,共4页Journal of Clinical Research
摘 要:[目的]探讨人C-反应蛋白(C-reactive protein,CRP)对急性肾损伤(AKI)自噬的影响.[方法]在术前2 h经腹腔注射25μg/mL体血容量(体血容量等于小鼠的克质量乘以0.08)的抗CD32抗体诱导小鼠体内人CRP的产生,然后构建急性肾缺血-再灌注损伤小鼠模型,分Sham组、野生型小鼠组(CRP-Wt-I/R组)、表达人CRP基因的转基因小鼠组(CRP-Tg-I/R组),比较肾缺血-再灌注损伤术前2h和术后0h、24h、72h小鼠体内CRP的变化,术后24h、72h时间点获取肾脏标本.HE染色后观察肾脏组织的病理变化,用免疫组化的方法检测自噬相关蛋白Beclin-1的表达情况,在透射电子显微镜下观察肾脏组织的自噬现象.[结果]小鼠肾缺血-再灌注损伤术后24 h、72 h时间点,CRP-Tg-I/R组肾小管上皮细胞Beclin-1蛋白的表达明显下降(P〈0.01),看不到自噬小体.[结论]人CRP下调AKI肾脏组织的自噬活性.[Objective]To invest the effect of human C- reactive protein on autophagy in acute kidney inju- ry . [Methods] In order to induce the production of human CRP in mice, 25 9 g/mL body volume was injected intraperitoneally 2 hours before operation (body blood volume was equal to the gram weight of mice multiplied by 0.08 ) of anti CD32 antibody, then the acute renal ischemia-reperfusion injury model was established in mice. The mice were divided into Sham group, wild type mice group (CRP-Wt-I/R group) and transgenic mice expressing human CRP gene group(CRP-Tg-I/R group); the changes of CRP in mice before and after renal ischemia-reperfusion injury 2 hours before and Oh,24h.72h after operation were compared, Kidney specimens were obtained at 24 h and 72 h after operation. After HE staining, the pathological changes of renal tissue were observed, the expression of autophagy associated protein Beclin-1 was detected by immunohistochemical meth- od, and the autophagy of renal tissue was observed under transmission electron microscope.[Results]At 24 hours and 72 hours after renal ischemia-reperfusion injury, the expression of Beclin-1 protein in renal tubular epithelial cells of the CRP-Tg-I/R group decreased significantly ( P〈0.01), and no autophagy was observed. [Conclusion]Human CRP down-regulated autophagy activity in renal tissue of AKI.
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