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冠心康对实验性大鼠急性心肌缺血的保护作用 被引量:3

Protective Effect of Guanxinkang Capsule against Myocardium Injury Induced by Acute Ischemia in Rats
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摘要 目的:探讨冠心康颗粒对大鼠急性心肌缺血的保护作用及其机理。方法:雄性大鼠32只,随机分为4组,每组8只,预防给药7d。灌胃结束后,采用在体大鼠冠状动脉左前降支结扎的方法建立心肌缺血模型,观察冠心康颗粒对大鼠急性心肌缺血后心肌中NO和NOS含量的影响,用免疫组化法检测Bc l-2蛋白在心肌中的表达。结果:模型组、冠心康组、地奥组与假手术组比较,心肌组织NO及NOS含量均有明显降低(P<0.05);而与模型组相比,冠心康组、地奥组的NO及NOS含量均有明显的恢复(P<0.05),提示冠心康颗粒可明显提高大鼠急性心肌缺血后心肌中NO和NOS含量(P<0.005,0.005),同时增加Bc l-2蛋白的表达,减少细胞凋亡。结论:冠心康颗粒对大鼠急性心肌缺血具有保护作用,可能与其提高心肌中NO和NOS含量,增加Bc l-2蛋白的表达有关。 Objective : To explore the effect and mechanism of Guanxinkang Capsule against myocardium injury induced by acute ischemia in rats. Methods :32 male rats were randomly divided into 4 groups,8 in every group. After fedding Guanxinkang Capsule for 7 dags preventedly, to ligate forward - descending branch of left coronary artery, establish the injured model and observe the changes of NO and NOS of myocardium. The myocardial expression of Bel -2 was detected by immunohistochemistry. Results :NO and NOS of myocardium apparentedly decreased in model group,Guanxinkang Capsule group and Diao group( P 〈 0.05 ). NO and NOS of Guanxinkang Capsule group and Diao group apparentedly recovery to model group( P 〈 0.05 ). This prompted that Guanxinkang Capsule could increase NO and NOS of myocardium in isehemia rats( P 〈 0. 005,0.005 ) and increase myocardial Bcl -2 protein expression,inhibit myocardial apoptosis. Conclusion :the effect of Guanxinkang Capsule against myocardium injury induced by acute isehemia in rats may have relationship with increasing NO and NOS of myocardium and expression of Bcl - 2 protein.
出处 《中医药学刊》 CAS 2006年第2期238-241,共4页 Study Journal of Traditional Chinese Medicine
基金 国家科技部新药基金项目(96-901-05-222)
关键词 冠心康颗粒 心肌缺血 一氧化氮 一氧化氮合酶 细胞凋亡 BCL-2 Guanxinkang Capsule myocadinm injury induced by acute ischemia NO NOS myocardial apoptosis Bcl - 2
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参考文献7

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二级参考文献2

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