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卡托普利和螺内酯合用对家兔心肌缺血再灌注损伤细胞凋亡的影响 被引量:3

Effect of Spironolactone and Captopril on Cardiomyocyte Apoptosis During Ischemic and Reperfution Period
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摘要 目的探讨卡托普利和螺内酯合用对心肌缺血再灌注损伤细胞凋亡的影响。方法50只新西兰家兔随机分为五组:假手术组、缺血再灌注组及缺血再灌注前分别应用螺内酯、卡托普利和卡托普利+螺内酯。模型制备结扎左心室支远端45 min,再灌注4 h。免疫组织化学观察Bcl-2和Bax的表达,缺口末端标记法检测细胞凋亡阳性率。结果Bcl-2和Bax在各组表达不相同,各组间比较差异显著。Bcl-2在卡托普利组和螺内酯组表达阳性率明显高于缺血再灌注组,而在卡托普利+螺内酯组表达阳性率明显高于卡托普利组和螺内酯组。Bax在卡托普利组和螺内酯组表达阳性率明显低于缺血再灌注组,而在卡托普利+螺内酯组表达阳性率明显低于卡托普利组和螺内酯组。卡托普利组和螺内酯组细胞凋亡程度明显低于缺血再灌注组,而卡托普利+螺内酯组细胞凋亡程度明显低于卡托普利组和螺内酯组。结论螺内酯和卡托普利合用可减轻缺血再灌注心肌细胞凋亡程度。 Aim To investigate effect of Captopril ( CAP ) and Spironolactone (SPI) on cardiomyocyte apoptosis during ischemic and reperfution (I/R) period. Methods Fifty New Zealand rabbits were randomly separated into five groups. Sham-operate group ( n = 10 ) was established without coronary artery ligation. I/R model was established by tighting two thread which went through Numier pipe for 45 minutes, then unclamped and reperfused for 4 hours. The SPI group ( n = 10) was established in the same way of I/R group with SPI (5 mg/( kg · d) ,bid) interference in a preoperative week. The CAP group was established with CAP ( 10 mg/( kg · d) , bid) as the SPI group' s. The CAP + SPI group was done with (SPI 5 mg/( kg · d ) and CAP 10 mg/( kg · d ) , bid ). The expression of Bcl-2 and Bax protein in cardiomyocyte was examined using immuno-histochemistry. The cardiomyoeyte apoptosis was examined by TUNEL. Results The expression rate of Bcl-2 protein in the CAP + SPI group was higher than that in CAP group, SPI group and I/R group, while the Bax was lower than that in other groups. The cardiomyocyte apoptosis was lower in the CAP + SPI group than that in the other groups. Conclusion Spironolactone and captopril may protect cardiomyocyte from I/R injury by decreasing their apoptosis.
出处 《中国动脉硬化杂志》 CAS CSCD 北大核心 2009年第1期27-30,共4页 Chinese Journal of Arteriosclerosis
基金 江苏省社会发展基金(BS2002009) 江苏省高校省级重点实验室开放课题(KJS04006)
关键词 缺血再灌注损伤 螺内酯 卡托普利 细胞凋亡 Ischemia/Reperfusion Injury Spironolactone Captopril Apoptosis
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参考文献8

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