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冠状动脉闭塞后Fas表达与细胞凋亡之间的时空解离

Tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion.

作者信息

Feng Q Z, Li T D, Wei L X, Qiao X, Yi J, Wang L, Yang T S

机构信息

Department of Cardiology, General Hospital of Chinese PLA, 28 Fuxing Road, Beijing 100853, China.

出版信息

Mol Pathol. 2003 Dec;56(6):362-7. doi: 10.1136/mp.56.6.362.

Abstract

AIMS

To explore the role of Fas in cardiomyocytic apoptosis induced by ischaemia through determining the histological relation between Fas expression and apoptosis in rat myocardium during ischaemia/infarction.

METHODS

The myocardial ischaemia model was produced by ligating the left coronary artery in Sprague-Dawley rats. The rats were killed from 10 minutes to seven days after surgery. Apoptotic myocardial cells were detected by the in situ terminal deoxynucleotidyl transferase mediated nick end labelling method, and the expression of Fas by immunohistochemistry and western blotting.

RESULTS

Cardiomyocytic apoptosis appeared from three to 36 hours after ischaemia. The expression of Fas could be detected by western blot from before surgery to seven days of ischaemia. Apoptosis and the expression of Fas in the cardiomyocytes appeared in different regions of the myocardium: apoptosis in the ischaemic region, Fas in the regions surrounding ischaemic myocardium.

CONCLUSION

These results suggest that there is a tempero-spatial dissociation between the expression of Fas and apoptosis after coronary occlusion. Fas might not directly regulate the apoptosis of cardiomyocytes induced by ischaemia.

摘要

目的

通过确定大鼠心肌缺血/梗死期间Fas表达与凋亡之间的组织学关系,探讨Fas在缺血诱导的心肌细胞凋亡中的作用。

方法

通过结扎Sprague-Dawley大鼠的左冠状动脉制备心肌缺血模型。术后10分钟至7天处死大鼠。采用原位末端脱氧核苷酸转移酶介导的缺口末端标记法检测凋亡心肌细胞,采用免疫组织化学和蛋白质印迹法检测Fas的表达。

结果

缺血后3至36小时出现心肌细胞凋亡。术前至缺血7天,通过蛋白质印迹法可检测到Fas的表达。心肌细胞中的凋亡和Fas表达出现在心肌的不同区域:缺血区域出现凋亡,缺血心肌周围区域出现Fas。

结论

这些结果表明冠状动脉闭塞后Fas表达与凋亡之间存在时空分离。Fas可能不直接调节缺血诱导的心肌细胞凋亡。

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Overexpression of Bcl-2 attenuates apoptosis and protects against myocardial I/R injury in transgenic mice.
Am J Physiol Heart Circ Physiol. 2001 May;280(5):H2313-20. doi: 10.1152/ajpheart.2001.280.5.H2313.

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