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目的探讨促红细胞生成素(EPO)预处理对大鼠缺血性急性肾衰竭(ARF)的保护作用及可能机制。方法 24只SD大鼠建立缺血-再灌注(I-R)缺血45min,再灌注24h模型后,均分为I-R组(模型对照组)和(E+I-R组)(术前24h腹腔注射rhEPO 3000U/kg);另取24只SD大鼠均分为S组(假手术)和E组(腹腔注射rhEPO 3000U/kg,24h后实施假手术)。分别于缺血前及再灌注后测定大鼠血肌酐(SCr)和血尿素氮(BUN)值,HE染色及肾小管Paller法评分观察大鼠肾组织损伤形态学改变,TUNEL法检测肾小管上皮细胞凋亡,Western blot测定肾组织中B-细胞淋巴瘤/白血病2原癌基因(Bcl-2)和半胱天冬蛋白酶3(Caspase-3)蛋白表达。结果与I-R组比较,E+I-R组再灌注后SCr、BUN、肾小管paller评分和凋亡指数降低(P<0.05),Bcl-2蛋白表达上调,Caspase-3蛋白表达下调(P<0.05)。与缺血前相比,I-R组和E+I-R组再灌注后Bcl-2蛋白表达下调,而Caspase-3蛋白表达上调(P<0.05)。结论 EPO预处理对缺血性ARF有保护作用;其机制可能与上调Bcl-2蛋白表达、降低Caspase-3蛋白表达和抑制肾小管上皮细胞凋亡有关。
Objective To investigate the protective effect and possible mechanism of erythropoietin (EPO) preconditioning on acute renal failure (ARF) in rats. Methods Twenty-four Sprague-Dawley rats were randomly divided into three groups: IR group (model control group) and E + IR group (intraperitoneal injection of rhEPO 3000U for 24 hours after ischemia-reperfusion (IR) / kg); another 24 SD rats were divided into S group (sham operation) and E group (intraperitoneal injection of rhEPO 3000U / kg, 24h after sham operation). The levels of serum creatinine (SCr) and blood urea nitrogen (BUN) were measured before ischemia and after reperfusion. The morphological changes of renal tissue were observed by HE staining and Paller method. The renal tubular epithelial cells The protein expressions of Bcl-2 and Caspase-3 in B-cell lymphoma / leukemia 2 in renal tissues were detected by Western blot. Results Compared with the IR group, the levels of SCr, BUN, tubular paller score and apoptosis index decreased (P <0.05), Bcl-2 protein expression and Caspase-3 protein expression decreased . Compared with that before ischemia, Bcl-2 protein expression and Caspase-3 protein expression were up-regulated in I-R group and E + I-R group after reperfusion (P <0.05). Conclusion EPO preconditioning may protect ischemic ARF. The mechanism may be related to the up-regulation of Bcl-2 protein expression, the decrease of Caspase-3 protein expression and the inhibition of renal tubular epithelial cell apoptosis.