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目的:观察外源性骨髓间充质干细胞(Mesenchymal stem cells,MSCs)对庆大霉素(Gentamycin,GM)诱导的大鼠急性肾损伤是否具有治疗作用,并初探其机制。方法:建立腹腔注射庆大霉素致大鼠急性肾损伤模型实验分为正常对照组、模型组、MSCs治疗组(模型+MSCs)、生理盐水组(模型+生理盐水)。于不同处理后4d分别检测血尿素氮(BUN)和肌酐(Scr)水平,观察肾组织病理改变,免疫印迹及RT-PCR法检测肾组织肝细胞生长因子(Hepatocyte growth factor,HGF)水平。结果:模型组大鼠的BUN及Scr较正常对照组显著升高,且肾小管组织病理损伤严重;而MSCs治疗组大鼠的BUN及Scr水平较生理盐水组显著降低,肾小管组织病理损伤明显减轻。此外,促肾小管损伤修复的肝细胞生长因子(HGF)表达在MSCs治疗组显著高于生理盐水组。结论:MSCs输注可促进庆大霉素所致急性肾小管损伤的修复,改善肾功能,其作用机制可能是与上调肾组织中肝细胞细胞生长因子的表达有关。
OBJECTIVE: To observe whether exogenous bone marrow mesenchymal stem cells (MSCs) have a therapeutic effect on acute renal injury induced by gentamycin (GM) in rats and to explore its mechanism. Methods: The model of acute renal injury induced by gentamicin in rats was established by intraperitoneal injection. The experiment was divided into normal control group, model group, MSCs treatment group (model + MSCs) and saline group (model + saline). Blood urea nitrogen (BUN) and creatinine (Scr) levels were measured 4 days after treatment. The pathological changes of renal tissues were observed. The levels of hepatocyte growth factor (HGF) in renal tissues were detected by Western blotting and RT-PCR. Results: The levels of BUN and Scr in model group were significantly higher than those in normal control group, and the histopathological damage of renal tubules was serious. The levels of BUN and Scr in MSCs-treated group were significantly lower than those in saline group Reduce. In addition, the expression of hepatocyte growth factor (HGF) promoted by renal tubular injury was significantly higher in the MSCs-treated group than in the saline group. CONCLUSION: MSCs infusion can promote the repair of acute tubular injury induced by gentamicin and improve the renal function. Its mechanism may be related to the up-regulation of hepatocyte growth factor expression in renal tissues.