肾损伤分子-1在肾小管上皮细胞缺氧损伤中的保护作用  

KIM-1 protects renal tubular epithelial cells from hypoxic injury

作　　者：霍文谦[1] 张克勤[1] 

机构地区：[1]第三军医大坪医院野战外科研究所泌尿外科,重庆400042

出　　处：《重庆医学》2015年第17期2308-2310,共3页Chongqing medicine

基　　金：第三军医大学青年人才创新基金资助(2010XQN30)

摘　　要：目的观察肾损伤分子-1(KIM-1)对肾小管上皮细胞缺氧损伤时增殖及凋亡的影响,证实KIM-1对肾缺氧损伤的保护作用。方法以人近端肾小管上皮细胞HK-2为研究对象,用pcDNA-hKIM-1质粒转染HK-2细胞,获得稳定表达KIM-1的pcDNA-hKIM-1-HK2细胞株。观察pcDNA-hKIM-1-HK2细胞(A组)和KIM-1抗体预处理pcDNA-hKIM-1-HK2细胞(C组)在缺氧损伤后细胞活力、凋亡指标及凋亡相关信号分子表达,以未转染缺氧HK-2细胞(B组)作为对照。结果 A组细胞活力指数高于B组(0.427±0.046 vs.0.210±0.036,P<0.05),细胞凋亡数量及流式细胞仪检测的缺氧早、晚期凋亡指数明显低于B组(P<0.05)。A组细胞缺氧时磷酸化ERK、磷酸化Akt表达较C组明显升高(P<0.05)。结论 KIM-1对肾小管上皮细胞缺氧损伤具有保护作用,其机制与激活PI3K-Akt/PKB和ERK信号通路抑制凋亡有关。Objective To demonstrate the protective effect of Kidney injury molecule-l（KIM-1） on kidney hypoxic injury by observing the effect of KIM-1 on the proliferation and apoptosis of HK2 ceils following hypoxic injury. Methods Human proximal kidney tubular epithelial ceils （HK-2） were used in this study. The pcDNA-hKIM-1 plasmids were transfected into HK2 cells for obtaining pcDNA-hKIM-1-HK2 cell strain that stably expressed KIM-1. Cell viability,apoptosis and expression of apoptosis related signal molecules of pcDNA-hKIM-1-HK2（group A） and pcDNA-hKIM-1-HK2 pretreated by KIM-1 antibody（group C） were observed after hypoxic injury,and compared with the untransfected HK2（group B）. Results The proliferation ability of group A was higher than the group B（0. 427±0. 046 vs. 0. 210±0. 036 ,P〈0. 05）. The number of apoptotic cells and the apoptosis index deter- mined by flow cytometry at early,middle and late hypoxic stages were obviously lower in the group A than in group B（P〈0.05）. The expression of phosphorylated ERK and phosphorylated Akt in group A increased significantly comparing with group C（P〈0.05）. Conclusion KIM-1 can protect renal tubular epithelial cells from hypoxic injury,and KIM-1 may suppress apoptosis through the activation of PI3K-AKt/PKB and ERK signal pathways.

关 键 词：肾损伤分子1 肾小管上皮细胞 缺氧损伤 保护效应 

分 类 号：R692[医药卫生—泌尿科学]