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依达拉奉对心肺复苏后大鼠肾损伤的保护作用及其机制 被引量:7

Protective mechanism of edaravone against rats with kidney injury after cardiopulmonary resuscitation
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摘要 目的探讨依达拉奉对心肺复苏后大鼠肾脏的保护作用及其机制。方法将36只SD大鼠随机分为假手术组、复苏对照组和依达拉奉组,建立大鼠心跳骤停.心肺复苏模型,复苏后24h检测血清尿素(SU)和肌酐(Scr),观察肾小管上皮细胞凋亡并检测肾组织bax和bcl-2的mR.NA表达。结果依达拉奉组SU[(11.52±2.67)比(17.70±3.36)mmol/L]、Scr[(72.36±6.78)比(92.58±10.47)μmol/L]、凋亡细胞数(7.32±0.97比8.91±1.41)和bax mRNA(4.59±0.73比8.43±0.72)均低于复苏对照组;bcl-2 mRNA(8.35±0.72比5.83±0.61)较复苏对照组增强。结论依达拉奉可以保护心肺复苏后大鼠肾功能,其机制与调节bcl-2和bax基因表达从而减轻肾小管上皮细胞凋亡有关。 Objective To investigate the protective effects and its mechanism of edaravone against rats with kidney injury after cardiopulmonary resuscitation. Methods Rats were randomly divided into sham group,resuscitation group, and edaravone group, with 12 rats in each group. Rat cardiac arrest- cardiopulmonary resuscitation model was established. Twenty-four h after resuscitation, serum levels of urea and creatinine were determined, apoptosis of renal tubule epithelium was assessed by TUNEL, and the expression of bax mRNA and bcl-2 mRNA was detected by RT-PCR. Results In edaravone group, serum levels of urea [ ( 11.52 ± 2.67) vs ( 17.70 ± 3.36) mmol/L] and creatinine [ (72.36 ±6.78 ) vs (92.58 ±10.47 ) μmol/L ], number of apoptotic cells (7.32 ± 0.97 vs 8.91 ± 1.41 ), and the expression of bax mRNA (4.59 ±0.73 vs 8.43± 0.72) were lower than those in resuscitation group, and expression of bcl-2 mRNA was higher than that in resuscitation group (8.35± 0.72 vs 5.83 ±0.61 ). Conclusion Edaravone can protect renal function in rats after cardiopulmonary resuscitation, partly through inhibition of cell apoptosis by regulating the expression of bcl-2 mRNA and bax mRNA.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2009年第6期778-779,共2页 Chinese Journal of Experimental Surgery
关键词 依达拉奉 心肺复苏 肾损伤 脱噬作用 Edaravone Cardiopulmonary resuscitation Kidney injury Apoptosis
作者简介 通信作者:祝禾辰
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