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中国临床药理学与治疗学 ›› 1998, Vol. 3 ›› Issue (3): 184-186.

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川芎嗪对大鼠心肌缺血再灌注损伤保护作用的研究

万福生, 赵小曼, 刘波, 李金生   

  1. 江西医学院生化教研室, 南昌330006
  • 收稿日期:1998-07-08 修回日期:1998-08-17 发布日期:2020-12-02
  • 作者简介:万福生, 男, 40 岁, 硕士, 副教授, 主要研究方面是心血管的细胞保护作用。

Protective effects of liqustrazin on myocardial ischemia-reperfusion injury in rats

WAN Fu-heng, ZHAO Xiao, Man LIU, Bo LI Jin-heng   

  1. Department of Biochemistry, Jiangxi Medical College, Nanchang 330006
  • Received:1998-07-08 Revised:1998-08-17 Published:2020-12-02

摘要: 目的 观察川芎嗪对心肌缺血再灌注损伤的保护作用及机理。方法 采用大鼠冠脉结扎30 min后再通20 min 造成心肌缺血再灌模型。大鼠随机分对照组、缺血组、模型组(缺血再灌组)和川芎嗪保护组。观测心肌细胞膜和线粒体中过氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH·PX)、Ca2+-ATP酶和K+, Na+-ATP 酶活力, MDA及心肌钙含量。结果 川芎嗪保护组心肌细胞膜SOD、GSH·PX、Ca2+-ATP 酶和Na+, K+-ATP酶活性较缺血再灌组均有显著性升高(P<0.05 或P <0.01), 丙二醛(MDA)和心肌钙含量却呈显著性降低。线粒体中SOD和GSH·PX 活力也呈显著性升高(P <0.05), MDA 却为显著性降低。结论 川芎嗪对大鼠缺血再灌注损伤心肌有确切保护作用, 其机理是通过提高对氧自由基的清除及抑制脂质过氧化。

关键词: 川芎嗪, 心肌, 缺血再灌注损伤, 氧自由基, 腺苷三磷酸酶类, 脂质过氧化物

Abstract: Aim The effect of liqustrazin on myocardial ischemia leperfusion injury in rats was observd. Methods The rat model of myocardial ischemia tepeifusion was established by ligating coro-nary artery. The rats were randomly divided in the control, model and liqustrazin treated groups. The activities of SOD, GSH · PX, Ca2+-ATPase, K+, Na+ ATPase and contents of MDA and Ca2+ were observed respectively. Results In the liqustrazin treated group as compared with those of the model, the activities of SOD, GSH · PX, Ca2+ ATPase, K+, Na+ -ATPase in the myocardial membrane increased significantly (P <0.01 or P <0.05) w hile contents of MDA and Ca2+ decreased (P <0.01) significantly. Activities of SOD and GSH · PX in the mitochondria was also increased (P <0.01) and MDA content decreased (P <0.01). Conclusions Liqustrazin has notable protective effects on myocardial-ischemia leperfusion injury in rats, which is due to its scarenging oxygen free radicals and anti ipid peroxydation reaction.

Key words: liqustrazin, myocardium, ischemia Teperfusion injury, oxy free radicals, adenosine triphosphatase, lipid peroxydation

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