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机构地区:[1]广州蛇毒研究所 [2]中山大学药学系
出 处:《中国中药杂志》1998年第9期556-557,共2页China Journal of Chinese Materia Medica
摘 要:目的:观察3种穿心草酮(Xan)对缺血再灌注模型心律失常的保护作用及其机制。方法:采用整体大鼠心肌缺血再灌注模型,于结扎前3miniv3种Xan1mg/kg。结果:3种Xan可不同程度地降低缺血再灌注损伤引起的室性心律失常发性率,缩短持续时间;提高超氧化物歧化酶(SOD)的活性,减少脂质过氧化反应代谢产物丙二醛的含量,减少心肌谷草转氨酶及乳酸脱氢酶的释放量;作用强度的顺序为:XanⅠ>XanⅢ>XanⅡ。结论:3种Xan具有抗心肌缺血再灌注损伤的保护作用,作用机制可能是与其降低心肌脂质过氧化及增强SOD的活性有关;Xan的活性与其苯环上羟自由基及甲氧基的多少及其位置有关。Objective:To study the protective effect of 1,8dihydroxy3,5dimethoxyxanthone (XanI)1hydroxy5dimethoxyxanthone(XamII)and 1hydroxy3,7,8trimethoxyanthone (XanIII)on arrhythmia induced by myocardial ischemiareperfusion injury and their mechanism.Method:A rat model was used .The experimental result shows thar.Result:An intravenous injection of XanI,XanII and XanIII 1mg/kg given 3 min before left coronary artery ligation reduces significantly the incidence of ventricular arrhythmia and its duration,diminishes the release of glutamic oxaloacetic transaminase and lactate dehydrogenase, elevates the activity of superoxide dismutase and reduces the amount of malondialdehyde.The potency of the above effect among 3 Xans is XanI>XanIII>XanII.Conclusion:It follows that the protective effect of Xans on myocardial ischemiareperfusion induced by arrhythmia might be associated with the reduction of myocardial lipid peroxidation and the enhancement of SOD activity, and the amount and site ofOH(hydroxy) and OCH3(methoxy)on the benzenoid structure may be related to the affinity of Xan.
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