Role of Diazoxide in mediating  NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles

沈诚; 范士志; 陈建明; 李志平; 李寒

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Role of Diazoxide in mediating NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles

更新时间：2026-01-09

- Role of Diazoxide in mediating NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles
- Journal of Army Medical University Vol. 29, Issue 9, Pages: 789-791(2007)
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  CLC： R322.11;R329.26;R972.4
- Published：2007
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沈诚,范士志,陈建明,李志平,李寒.二氮嗪预处理对缺血再灌注大鼠心肌NF-κB和caspase-3表达的影响[J].陆军军医大学学报(原第三军医大学学报),2007,29(09):789-791.

　SHEN Cheng,FAN Shi-zhi,CHEN Jian-ming,LI Zhi-ping,LI Han.Role of Diazoxide in mediating NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(09):789-791.
沈诚,范士志,陈建明,李志平,李寒.二氮嗪预处理对缺血再灌注大鼠心肌NF-κB和caspase-3表达的影响[J].陆军军医大学学报(原第三军医大学学报),2007,29(09):789-791. DOI：

　SHEN Cheng,FAN Shi-zhi,CHEN Jian-ming,LI Zhi-ping,LI Han.Role of Diazoxide in mediating NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(09):789-791. DOI：

摘要

目的研究二氮嗪(Diazoxide

DZ)开放线粒体ATP敏感性钾通道对缺血再灌注损伤所致大鼠心肌组织NF-κB和caspase-3表达的影响。方法采用离体工作心脏灌注模型，大鼠随机分为正常对照组，缺血再灌注组，DZ治疗组

DZ抑制剂-格列苯脲组。采用TUNEL 法检测心肌细胞凋亡，Western印迹法测定心肌NF-κB活性

酶标法测caspase-3活性。结果 DZ组大鼠心肌细胞凋亡指数明显低于I/R组

高于对照组。与正常对照组相比

心肌组织NF-κB和caspase-3活性在缺血再灌注后有显著性增加(P0.01)。DZ处理后

NF-κB和caspase-3活性与缺血再灌注组相比有明显下降(P0.01)；格列苯脲组NF-κB和caspase-3活性明显高于DZ治疗组(P0.01)。结论心肌缺血再灌注损伤使凋亡指数，NF-κB和caspase-3活性明显升高

二氮嗪(DZ)开放线粒体ATP敏感性钾通道可下调心肌组织NF-κB和caspase-3的表达

这可能有助于减轻缺血再灌注所致心肌细胞凋亡的发生。

Abstract

Objective To investigate the effect of Diazoxide in mediating NF-κB and caspase-3 during ischemia-reperfusion in rat cardiac muscles. Methods Isolated rat heart model was used in our experiment. Forty male SD rats were randomly divided into normal control group

ischemia-reperfusion group

Diazoxide treatment group

Diazoxide inhibitor group (n=10 in each group). The apoptosis index of cardiac myocytes was detected by TUNEL. The expression NF-κB was measured by Western blotting. Caspase-3 levels in myocardium were measured by using fluorescent assay. Results The apoptosis index in DZ group was significantly lower than that in ischemia-reperfusion group

but higher than that in control group. NF-κB level in nucleus significantly increased after ischemia-reperfusion and caspase-3 activity had the same change. Treatment of Diazoxide significantly inhibited NF-κB level in nucleus

and concomitantly decreased the activity of caspase-3 in myocardium. The Diazoxide inhibitor could significantly increase the expression of NF-κB and the activity of caspase-3. Conclusion Myocardial ischemia-reperfusion can result in intensive activation of NF-κB and caspase-3. Early treatment with Diazoxide might attenuate myocardial injury induced by ischemia-reperfusion and relieve the apoptosis of cardiac myocytes.

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