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目的:探讨缺血预适应(IPC)介导内皮祖细胞(EPCs)归巢对保留肾单位手术(NSS)后肾功能的保护作用。方法:SD大鼠随机分为对照组(sham)、保留肾单位组(NSS)、缺血预适应+保留肾单位组(IPC)。术后24 h分别留取大鼠外周血、肾脏组织。采用血生化、病理学观察肾功能改变;免疫荧光观察3组大鼠肾组织中EPCs归巢情况;免疫组化技术检测肾脏微血管新生;QPCR检测血管生成因子mRNA表达。结果:IPC可显著降低大鼠血肌酐水平及肾小管损伤评分(P<0.05),促进EPCs归巢至损伤肾脏组织。与sham组和NSS组相比,IPC组大鼠肾脏组织微血管新生显著增强(P<0.05),且基质细胞衍生因子1(SDF-1)mRNA表达升高(P<0.05)。结论:IPC可介导EPCs归巢至损伤肾脏,后者可能通过释放血管生成因子,促进肾脏微血管新生,达保护肾功能之目的。
Objective: To investigate the protective effects of ischemic preconditioning (IPC) on the renal function of homing endothelial cells (EPCs) after nephron sparing (NSS). Methods: SD rats were randomly divided into sham group, NSS group and IPC group. Twenty four hours after operation, the peripheral blood and kidneys of rats were collected. The changes of renal function were observed by blood biochemistry and histopathology. The homing of EPCs in the kidney of the three groups was observed by immunofluorescence. The neovascularization was detected by immunohistochemistry. The mRNA expression of angiogenesis was detected by QPCR. Results: IPC can significantly reduce the level of serum creatinine and renal tubular injury score (P <0.05), and promote the homing of EPCs to the injured kidney tissue. Compared with sham group and NSS group, the neovascularization of kidneys in IPC group was significantly increased (P <0.05), and the expression of SDF-1 mRNA increased (P <0.05). Conclusion: IPC can mediate the homing of EPCs to injured kidneys. The latter may promote neovascularization of kidneys by releasing angiogenic factors and protecting renal function.