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作 者:范治璐[1] 杜鑫[1] 李卫平[2] 张涛[1] 于洋[1] 鞠红卫[1]
机构地区:[1]大连医科大学附属第二医院泌尿外科,辽宁大连116027 [2]大连医科大学药理学教研室,辽宁大连116044
出 处:《大连医科大学学报》2009年第5期524-528,共5页Journal of Dalian Medical University
摘 要:[目的]探讨缺血后处理对大鼠肾缺血再灌注损伤影响。[方法]夹闭左侧肾动脉60 min后再灌注6 h法制备肾脏缺血再灌注损伤模型。雄性SD大鼠18只随机分为3组:缺血再灌注组(IR组,n=6),缺血后处理组(IPO组,n=6),假手术组(Sham组,n=6)。测定血肌酐(Cr)浓度、尿素氮(Bun),检测肾脏组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和髓过氧化物酶(MPO)活性;取左肾组织行HE染色,光镜下观察肾组织病理学改变,免疫组化法检测肾组织中NF-κB表达。[结果]与Sham组比较,IR组血Cr浓度和血Bun浓度上升,达到(93.02±13.44)μmol/L和(15.58±0.56)mmol/L(P<0.01),SOD活性下降为(185.87±17.68)U/mgprot(P<0.01),MDA含量和MPO活性增加分别达到(4.09±0.34)nmol/mgprot、(0.90±0.07)U/g(P<0.01)。与Sham组比较IPO组血Cr、Bun浓度、MPO活性差异有统计学意义(P<0.05),SOD活性和MDA含量差异无统计学意义;病理损伤明显,肾脏组织中NF-κB表达增强。与IR组比较,IPO组血Cr和血Bun浓度降低分别为(58.98±8.02)μmol/L(P<0.01)、(9.45±1.03)mmol/L(P<0.01),SOD活性升高为(230.90±9.19)U/mgprot(P<0.01),MDA含量降低为(3.67±0.20)nmol/mgprot(P<0.01),MPO活力降低为(0.78±0.06)U/g(P<0.01),病理损伤减轻,肾脏组织NF-κB表达减弱。[结论]缺血后处理对肾脏有保护作用,其机制与增强肾脏抗氧化能力,减轻肾脏组织炎性细胞浸润和抑制肾组织NF-κB表达有关。[Objective] To investigate the effects of ischemic postconditioning on the ischemia-reperfusion injury in rat kidney.[Methods]Eighteen male SD rats were randomly divided into three groups as follows:(1)IR group(n=6).(2)Ischemic postconditioning group(n=6)(3)Sham group(n=6): Rats underwent the same surgical procedure without obstruction for 1 h.At the end of reperfusion for 6 h,the blood urea nitrogen(Bun),blood creatinine concentrations(Cr)were measured,the ischemic left renal tissue was collected for the determination of the superoxide dismutase(SOD) activity,malondialdehyde(MDA)content,myeloperoxidase(MPO) activity and the expression of NF-κB;the changes of renal tissue were observed by microscope.[Results] The Bun,Cr,MPO activity were significantly higher in IR and IPO group than those in Sham group(P〈0.05).SOD activity was lower whereas the MDA content was higher in IR group than those inSham group(P〈0.05) and the expression of NF-κB in IR group was significantly stronger than that in Sham group.In IPO group the Bun,Cr,MDA and MPO were significantly lower whereas SOD activity was significantly higher(P〈0.01) than those in IR group(P〈0.05),the expression of NF-κB was weaker than that in IR group.[Conclusion]Ischemic postconditioning attenuates renal ischemia-reperfusiong injury in rats.The mechanism is related to the enhancement of renal tissue antioxidation,inhibite of the neutrophilinfiltration and of NF-κB expression.
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