肾损伤分子-1在肾小管上皮细胞缺氧损伤中的保护作用.pdf

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1、2308重庆医学2015年6月第44卷第17期·论著·doi：10．3969／j．issn．1671—8348．2015．17．002肾损伤分子一1在肾小管上皮细胞缺氧损伤中的保护作用霍文谦，张克勤△(第三军医大坪医院野战外科研究所泌尿外科，重庆400042)[摘要]目的观察肾损伤分子一1(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一1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一2为研究对象，用pcDNA-hKIM-1质粒转染HK一2细胞，获得稳定表达KIM一1的pcDNA-hKIM-1一HK2细胞株。观察pcDNA-hKIM—l—

2、HK2细胞(A组)和KIM一1抗体预处理pcDNA-hKIM-1一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一2细胞(B组)作为对照。结果A组细胞活力指数高于B组(O．427土0．046z；s．0．210±0．036，P

3、1；肾小管上皮细胞；缺氧损伤；保护效应[中图分类号]R699．2[文献标识码]A[文章编号]16718348(2015)17—2308—03KIM-1protectsrenaltubularepithelialcellsfromhypoxicinjuryHuoWenqian，ZhangKeqin(DepartmentofUrology，InstituteofSurgeryResearch，DapingHospital，ThirdMilitaryMedicalUniversity)[Abstract-]}ObjectiveTodemonstratetheprotecti

4、veeffectofKidneyinjurymolecule-1(KIM-1)onkidneyhypoxicinjurybyobservingtheeffectofKIM-1ontheproliferationandapoptosisofHK2cellsfollowinghypoxici~ury．MethodsHumanproximalkidneytubularepithelialceils(HK-2)wereusedinthisstudy．ThepeDNA-hKIM一1plasmidsweretransfectedintoHK2ceilsforobtainingpc

5、DNA-hKIM-1-HK2cellstrainthatstablyexpressedKIM-1．Cellviability，apoptosisandexpressionofapoptosisrelatedsignalmoleculesofpeDNA-hKIM-1一HK2(groupA)andpcDNA-hKIM-1一HK2pretreatedbyKIM-1antibody(groupC)wereobservedafterhypoxicinjury，andcomparedwiththeuntransfectedHK2(groupB)．ResultsTheprolife

6、rationabilityofgroupAwas。higherthanthegroupB(O．427士0．046vs．0．210士0．036，P

7、ngroupAincreasedsignificantlycomparingwithgroupC(P<0．05)．ConclusionKIM-1canprotectrenaltubularepithelialcellsfromhypoxicinjury，andKIM一1maysuppressapoptosisthroughtheactivationofPI3K—AKt／PKBandERKsignalpathways．[-Keywords]kidneyinjurymolecule-1；renaltubularepithelialcells；hypoxi