刺五加的心肌保护作用及其机制的研究(1)
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[摘要] 目的：研究刺五加对急性心肌缺血大鼠的心肌保护作用及可能机制。方法：将40只雄性Wistar大鼠随机分为假手术组，模型组，刺五加高、中、低剂量 (100、50、25 mg/kg) 组，每组各8只。采用结扎大鼠左冠状动脉前降支制备急性心肌梗死模型，观察刺五加对心肌缺血的保护作用；采用原位末端脱氧核糖核酸转移酶介导的d-UTP缺口末端标记(TUNEL)法检测刺五加对心肌缺血大鼠心肌细胞凋亡的影响；采用激光扫描共聚焦技术检测刺五加对细胞内游离钙离子浓度的变化。结果：高剂量刺五加可缩小心肌梗死面积(P<0.05)，改善缺血心肌的心功能，减少缺血心肌细胞凋亡(P<0.05)，对60 mmol/L KCl诱导的缺血细胞内游离钙离子浓度的升高有明显抑制作用(P<0.05)。结论：刺五加对大鼠心肌缺血具有保护作用，其机制可能是通过下调细胞内游离钙离子浓度，抑制了心肌细胞凋亡。
[关键词] 刺五加；心肌梗死；共聚焦；游离钙离子
[中图分类号] R542.2 [文献标识码] A [文章编号] 1673-7210(2011)11(b)-023-03
Analysis of the myocardial protection effects and mechanism of Acanthopanax Senticosus
HUANG Wei, LI Guixia, XIE Yan, QI Hanping
Department of Pharmacology, Daqing Campus of Harbin Medical University, Heilongjiang Province, Daqing 163319, China
[Abstract] Objective: To investigate the protective effect of Acanthopanax Senticosus against myocardial ischemia and detect the possible mechanisms. Methods: 40 cases of male Wistar rats were divided into sham group, model group, low dose, middle dose and high dose Acanthopanax Senticosus group (100, 50, 25 mg/kg), each of 8 cases. The protective effects of Acanthopanax Senticosus on myocardial ischemia were observed by models of acute myocardial infarction which were operated with permanent ligation of left anterior descending coronary artery in rats. Myocardium apoptosis was measured by TUNEL. Laser scanning confocal microscopy was utilized to assay the effect of Acanthopanax Senticosus on intracellular calcium concentration. Results: In the high dose Acanthopanax Senticosus group, infarct size of myocardium decreased (P<0.05), heart function of ischemic myocardium improved (P<0.05), apoptosis of ischemia cardiac myocytes was inhibited (P<0.05), and intracellular calcium concentration decreased markedly which was induced by 60 mmol/L KCl (P<0.05). Conclusion: Acanthopanax Senticosus possesses protective effect on myocardial ischemia of rats. The possible mechanisms of myocardial ischemia are due to the decrease of intracellular calcium concentration and the inhibition of cardiac myocytes apoptosis ......
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