缺血后处理对止血带休克致肾损伤的作用  

Effect of ischemic postconditioning on kidney injury caused by tourniquet shock

作　　者：赵利军 李开济 吴静 门秀丽 

机构地区：[1]华北理工大学基础医学院病理生理学系,唐山063000 [2]唐山市慢性病临床基础研究重点实验室

出　　处：《山西医科大学学报》2017年第4期328-332,共5页Journal of Shanxi Medical University

基　　金：河北省卫生厅医学研究重点课题资助项目(20130060)

摘　　要：目的观察缺血后处理对止血带休克致肾损伤的作用,并探讨其可能机制。方法 30只SD大鼠随机分为对照组(Control组)、止血带休克组(TOS组)和缺血后处理组(I-postC组)。止血带法制作止血带休克动物模型,另对I-postC组动物在止血带休克基础上实施缺血后处理。经腹主动脉取血测各组大鼠血浆肌酐(Cr)、尿素氮(BUN)、C反应蛋白(CRP)水平;肾组织匀浆测组织SOD、MDA、XOD和MPO水平;免疫组化法检测肾组织细胞凋亡相关蛋白Bcl-2及Bax的表达;TUNEL法检测肾细胞凋亡;电镜下观察肾组织超微结构改变。结果 (1)与Control组比较,后两组肾组织SOD活力明显降低(P<0.01),血浆Cr、BUN、CRP均升高(P<0.01);肾组织MDA、XOD和MPO升高,差异具有统计学意义(P<0.05或P<0.01);免疫组化检测中Bax蛋白表达增强而Bcl-2蛋白表达略增强;TUNEL法检测可见肾细胞凋亡数目增多;透射电镜下可见肾近曲小管上皮细胞核固缩,胞内空泡,溶酶体和致密颗粒沉积增多,部分线粒体嵴断裂或模糊。肾小球足突细胞突起不规则、融合,线粒体嵴断裂并减少,有空泡,粗面内质网扩张。(2)与TOS组比较,I-postC组肾组织SOD活性增强,血浆Cr、BUN、CRP及肾组织MDA、XOD、MPO等相关损伤指标均有所下降,差异具有显著性(P<0.05或P<0.01);Bcl-2蛋白表达增强而Bax减弱,肾凋亡细胞数目减少。电镜下观察可见肾小管上皮细胞及肾小球毛细血管内皮细胞损伤程度减轻。结论肢体长时间应用止血带可导致肾功能障碍和肾组织结构损伤,缺血后处理可通过减少氧自由基生成和抑制炎症反应,减轻肾损伤。Objective To investigate the effects of ischemic postconditioning（I-postC） on kidney injury caused by tourniquet shock,and explore its possible mechanisms. Methods Thirty SD rats were randomly divided into control group,tourniquet shock group（TOS group） and I-postC group. The tourniquet shock animal models were induced by tourniquet. In I-postC group,ischemic postconditioning was performed based on the treatment in model group. Blood was taken from the abdominal aorta to measure the contents of blood creatinine（Cr）,blood urea nitrogen（BUN） and C-reactive protein（CRP） in plasma. The contents of superoxide dismutase（SOD）,malondialdehyde（MDA）,xanthine oxidase（XOD）,and myeloperoxidase（MPO） in renal tissues were determined. The expression of Bcl-2 protein and Bax protein in renal tissue was detected. The apoptotic cells in renal tissue were determined by terminal-deoxynucleotidyl transferase-mediated d-UTP nick end labeling（TUNEL）. The histological ultrastructure changes of renal tissues were observed under electron microscope. Results（1）Compared with control group,SOD activity in renal tissues reduced in TOS group and I-postC group（P〈0. 01）,while the levels of Cr,BUN and CRP in plasma increased（P〈0. 01）,and the levels of MDA,XOD,MPO in renal tissues also increased（P〈0. 01）. Compared with control group,Bax protein expression increased obviously in TOS group and I-postC group,and the antiapoptotic gene Bcl-2 expression increased slightly. The number of renal tubular epithelial cells and endothelial cell apoptosis increased in TOS group and I-postC group. Under the transmission electron microscope,there were renal proximal convoluted tubule epithelial cell nucleus pycnosis,intracellular cavitation,increased lysosome and dense particle deposition,and some mitochondria crest fracture or fuzzy. Glomerular podocyte protuberant,irregular,fusion,mitochondrial cristae fracture and reduced free bubble,rough endoplasmic reticulum expansion were also observed.（2）Co

关 键 词：止血带休克 肾损伤 缺血后处理 细胞凋亡 

分 类 号：R363[医药卫生—病理学]