系统医学2024,Vol.9Issue(8) :192-194,198.DOI:10.19368/j.cnki.2096-1782.2024.08.192

抑制炎性小体活化对大鼠心肌缺血的作用研究

Effect of Inhibiting Inflammasome Activation on Myocardial Ischemia in Rats

何莉 黎文博 廖思涵 彭华
系统医学2024,Vol.9Issue(8) :192-194,198.DOI:10.19368/j.cnki.2096-1782.2024.08.192

抑制炎性小体活化对大鼠心肌缺血的作用研究

Effect of Inhibiting Inflammasome Activation on Myocardial Ischemia in Rats

何莉 1黎文博 2廖思涵 1彭华1
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作者信息

  • 1. 湖南交通工程学院,湖南衡阳 421000
  • 2. 湖南食品药品职业学院,湖南长沙 410208
  • 折叠

摘要

冠状动脉粥样硬化性心脏病(简称冠心病)发病率持续升高,严重危害居民身心健康.冠状动脉粥样硬化所造成的冠状动脉狭窄或闭塞是诱发心肌缺血最常见、最关键的病因.心脏损伤和愈合的主要机制是炎症发生发展过程.过度炎症反应使不良心室重构.研究证实,Nod样受体蛋白(Nod-like Receptor Protein,NLRP)3炎性小体介导的炎症反应能够参与冠状动脉硬化、急性心肌梗死、缺血/再灌注损伤及房颤后心脏重构的过程,正确抑制NLRP3炎性小体的激活机制,可减缓炎症反应发生发展和抑制细胞焦亡,有效防治心血管疾病.抑制炎性小体活化在一定程度上能够减轻心肌缺血坏死状况.

Abstract

The incidence of coronary atherosclerotic heart disease(CHD)continues to rise,seriously endangering the physical and mental health of residents.Coronary artery stenosis or occlusion caused by coronary atherosclerosis is the most common and critical cause of myocardial ischemia.The main mechanism of cardiac injury and healing is inflam-mation.Excessive inflammation leads to poor ventricular remodeling.Studies have confirmed that Nod-like receptor protein 3(NLRP)inflammasome mediated inflammation can participate in the process of coronary arteriosclerosis,acute myocardial infarction,ischemia/reperfusion injury and cardiac remodeling after atrial fibrillation.Correctly in-hibiting the activation mechanism of NLRP3 inflammasome can slow down the occurrence and development of inflam-matory response,inhibit apoptosis,and effectively prevent and treat cardiovascular diseases.Inhibition of inflamma-some activation can alleviate myocardial ischemic necrosis to a certain extent.

关键词

炎性小体/心肌缺血/冠状动脉粥样硬化

Key words

Inflammasome/Myocardial ischemia/Coronary atherosclerosis

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基金项目

湖南省教育厅科研项目(22C0944)

出版年

2024
系统医学

系统医学

ISSN:
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