刘艳, 荆玉红, 孙宏丽, 李呼伦, 杨宝峰. M3受体与大鼠缺血性心肌细胞凋亡关系的研究M3受体与大鼠缺血性心肌细胞凋亡关系的研究J. 药学学报, 2004, 39(5): 338-341.
引用本文: 刘艳, 荆玉红, 孙宏丽, 李呼伦, 杨宝峰. M3受体与大鼠缺血性心肌细胞凋亡关系的研究M3受体与大鼠缺血性心肌细胞凋亡关系的研究J. 药学学报, 2004, 39(5): 338-341.
LIU Yan, JING Yu-hong, SUN Hong-li, LI Hu-lun, YANG Bao-feng. Relationship between M3 receptor and myocyte apoptosis induced by acute myocardial infarctionJ. Acta Pharmaceutica Sinica, 2004, 39(5): 338-341.
Citation: LIU Yan, JING Yu-hong, SUN Hong-li, LI Hu-lun, YANG Bao-feng. Relationship between M3 receptor and myocyte apoptosis induced by acute myocardial infarctionJ. Acta Pharmaceutica Sinica, 2004, 39(5): 338-341.

M3受体与大鼠缺血性心肌细胞凋亡关系的研究M3受体与大鼠缺血性心肌细胞凋亡关系的研究

Relationship between M3 receptor and myocyte apoptosis induced by acute myocardial infarction

  • 摘要: 目的观察M3受体对大鼠缺血性心肌细胞凋亡的作用及其机制。方法结扎大鼠左冠状动脉前降支建立急性心肌缺血模型,给予M3受体激动剂胆碱或阻断剂4DAMP进行干预,观察M3受体对其的影响。结果缺血前15 min iv胆碱10 mg·kg-1可提高血清超氧化物歧化酶(SOD)活力,降低丙二醛(MDA)含量,减少凋亡细胞的数量(P<0.01),并可增加Bcl-2表达,减少Fas表达。预先5 min iv 4DAMP 0.12 mg·kg-1阻断心肌M3受体可逆转胆碱的作用。结论激动M3受体对结扎大鼠冠状动脉诱导的心肌损伤有保护作用,其机制可能与调节Bcl-2和Fas表达从而抑制心肌细胞凋亡有关。

     

    Abstract: AimTo explore the effects of M3 receptor on myocyte apoptosis induced by acute myocardial infarction in rats. MethodsRat model was induced by ligation of the anterior branch of the left coronary artery. All animals were divided into four groups: sham-operated group, occlusion group, choline group (10 mg·kg-1, iv), and 4DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) group (0.12 mg·kg-1, iv). The serum malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. The infarct size areas on the myocardium were identified by TTC staining. The apoptosis in cardiomyocyte was detected by TUNEL assay and apoptosis-related proteins in Bcl-2 and Fas expression were measured by immunohistochemistry assay. ResultsM3 receptor agonist choline reduced serum MDA content and increased SOD activity. The myocardial expression of Bcl-2 was increased, whereas the expression of Fas was decreased by choline. However, blockade of M3 receptor by 4DAMP completely inhibited these effects of choline on cardiac myocytes. ConclusionActivation of M3 receptor has protective effect on myocyte apoptosis induced by acute myocardial infarction in rat, and this effect might be related to modulating the expression of some immediate-early genes including Bcl-2 and Fas.

     

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