李庆林, 桂新, 陈志武, 马传庚. 金丝桃苷抑制大鼠心肌缺血再灌注损伤引起的细胞凋亡作用的机制J. 药学学报, 2002, 37(11): 849-852.
引用本文: 李庆林, 桂新, 陈志武, 马传庚. 金丝桃苷抑制大鼠心肌缺血再灌注损伤引起的细胞凋亡作用的机制J. 药学学报, 2002, 37(11): 849-852.
LI Qing-lin, CHOU Gui-xin, CHEN Zhi-wu, MA Chuan-geng. INHIBITORY MECHANISM OF HYPERIN ON THE APOPTOSIS IN MYOCARDIAL ISCHEMIA/REPERFUSION IN RATSJ. Acta Pharmaceutica Sinica, 2002, 37(11): 849-852.
Citation: LI Qing-lin, CHOU Gui-xin, CHEN Zhi-wu, MA Chuan-geng. INHIBITORY MECHANISM OF HYPERIN ON THE APOPTOSIS IN MYOCARDIAL ISCHEMIA/REPERFUSION IN RATSJ. Acta Pharmaceutica Sinica, 2002, 37(11): 849-852.

金丝桃苷抑制大鼠心肌缺血再灌注损伤引起的细胞凋亡作用的机制

INHIBITORY MECHANISM OF HYPERIN ON THE APOPTOSIS IN MYOCARDIAL ISCHEMIA/REPERFUSION IN RATS

  • 摘要: 目的研究金丝桃苷(hyperin,Hyp)对大鼠心肌缺血再灌注诱导的细胞凋亡的保护作用。方法用荧光显微镜和电子显微镜观察;原位末段标记法(TUNEL)和流式细胞术检测等。结果Hyp(25,50 mg·kg-1)对缺血30 min后再灌注3.5 h导致大鼠心肌细胞凋亡有保护作用;对培养的乳大鼠心肌细胞缺氧6 h再给氧24 h引起的细胞凋亡,Hyp(0.5~50.0 μmol·L-1)可以减少凋亡细胞的形成。结论金丝桃苷对缺血再灌注引起的大鼠心肌细胞损伤有保护作用;其作用机制可能与金丝桃苷抗心肌细胞凋亡有关。

     

    Abstract: AIMTo study the protective effect of hyperin on the apoptosis in rat cardiomyocyte induced by ischemia and reperfusion injury. METHODSThe apoptosis in myocardium was subjected to 30 min coronary occlusion followed by 3.5 h of reperfusion in male Sprague-Dawley rats. It was provided by 6 h of anoxia followed by 24 h of reoxygenation in the cultured neonatal rat cardiomyocytes. The profile of apoptotic myocardium was observed by phase-contrast microscope, fluorescent micrograph and terminal deoxynucleotidyl transferase mediated dUTP-digoxigenin nick end-labeling (TUNEL) method. The apoptotic number in cardiomyocytes was examined by transmission electron microscopy and flow cytometry. RESULTSIn the apoptosis myocardium of ischemia/reperfusion rat, hyperin (25, 50 mg·kg-1) was shown to inhibit the increase of apoptotic cells of the myocardium (P<0.05, P<0.01); hyperin was (0.5~50.0 μmol·L-1) also shown to significantly decrease the percentage of apoptotic cells in cultured neonatal rat cardiomyocyte. CONCLUSIONHyperin may have protective effect against cardiomyocyte ischemia/reperfusion injury. Cardiomyocyte apoptosis may be involved in the mechanism.

     

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