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作 者:詹周兵[1] 沈华英[1] 施晓松[1] 金东华[1] 石永兵[1]
机构地区:[1]苏州大学附属第二医院肾脏病科,江苏省215004
出 处:《江苏医药》2014年第5期511-514,共4页Jiangsu Medical Journal
摘 要: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 explore the protective effect and its underlying mechanism of erythropoietin(EPO) pretreatment on ischemic acute renal failure (ARF) in rats. Methods Model of ischemia-reperfusion(I-R) ARF(ischemia for 45 min and reperfusion for 24 h) were estahlished in 24 adult SD rats, which were equally divided into groups of I-R(model control) and E+I-R (intraperitoneal injection of rhEPO 3000 U/kg at 24 h before ischemia). Another 24 SD rats were taken as groups of S(sham operated) and E(intraperitoneal injection of rhEPO 3000 U/kg at 24 h before sham operation). Serum creatinine(SCr) and blood urea nitrogen(BUN) were detected before ischemia and after reperfusion. Morphological changes of renal tissues were observed by Pallet score of renal tubules and HE staining. Apoptosis of renal tubular epithelial cell was detected by TUNEL. The expressions of B-cell lymphoma/leukemia-2 (Bcl-2) and Caspase-3 were detected by Western blot. Results Compared with group I-R,SCr,BUN,Paller score and apoptosis index were lower in group E+I-R(P〈0. 05), Bcl-2 expression was up-regulated and Caspase-3 expression was down-regulated after reperfusion in group E+I-R (P〈0. 05). Compared to before, Bcl-2 was down-regulation and Caspase-3 was up-regulated after reperfusion in groups of I-R and E + I-R (P〈0. 05). Conclusion EPO pretreatment has a protective effect on the kideny with I-R injury. The underlying mechanism may he related to the up-regulation of Bcl-2, down-regulation of Caspase-3 and inhibition of apoptosis of renal tubular epithelial ceil.
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