《生命科学》 2023, 35(11): 1527-1534

NLRP3炎症小体与心脏骤停复苏后心肌缺血再灌注损伤的研究进展

王丽凤¹ , 任　骏^2,*

¹新疆医科大学基础医学院生理学教研室，新疆地方病分子生物重点实验室， 乌鲁木齐 830000 ²复旦大学附属中山医院心血管病研究所，上海 200032

摘　要：

心脏骤停已成为世界范围内的重大公共卫生问题，及时有效的心肺复苏可以挽救生命，改善心脏骤停患者的预后。尽管心肺复苏技术取得了进步，但与心脏骤停相关的死亡率仍然很高。NLRP3 炎症小体是细胞内多种蛋白质构成的复合物，在先天免疫中起着重要作用。组织损伤后，NLRP3 炎症小体激活产生大量细胞因子如白细胞介素(IL)-1β 和IL-18，最终导致炎症性细胞死亡( 细胞焦亡)。虽然适度的炎症反应有利于损伤组织愈合，但过度的NLRP3 炎症小体激活会产生不利影响。NLRP3 炎症小体在大量心血管疾病(cardiovascular diseases, CVDs) 中发挥关键作用。心脏骤停和复苏后缺血再灌注损伤(I/R 损伤) 可以通过各种信号通路激活NLRP3 炎症小体。抑制NLRP3 炎症小体活性可以改善心脏骤停和复苏后缺血再灌注损伤。该文将讨论NLRP3 炎症小体在心脏骤停和复苏过程中对细胞损伤的作用，同时针对抑制NLRP3 炎症小体激活，改善心脏骤停和复苏后缺血再灌注损伤的治疗方法进行系统阐述。

通讯作者：任　骏 , Email:jrenuwyo@ 126.com

Progress on NLRP3 inflammasome in myocardial ischemia-reperfusion injury after cardiac arrest and resuscitation

WANG Li-Feng¹ , REN Jun^2,*

¹Department of Physiology, School of Basic Medical Sciences, Xinjiang Key Laboratory of Molecular Biology for Endemic Diseases, Xinjiang Medical University, Urumuqi 830000, China ²Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University, Shanghai 200032, China

Abstract:

Cardiac arrest is becoming a major public health threat around the globe. Effective and timely cardiopulmonary resuscitation (CPR) can significantly improve the prognosis for patients with cardiac arrest. Despite the recent advances in CPR techniques, the cardiac arrest-associated mortality rate still remains high. The NLRP3 inflammasome is a multiprotein complex composed of various cellular proteins with an important role in the governance of innate immunity. Following tissue injury, activation of NLRP3 inflammasome produces various cytokines, including interleukin (IL)-1β and IL-18, ultimately leading to inflammatory cell death (pyroptosis). Although the moderate inflammatory response may be beneficial for tissue healing following injury, excessive activation of NLRP3 inflammasomes can be detrimental. The NLRP3 inflammasome plays a crucial role in numerous cardiovascular diseases (CVDs). Ischemia and reperfusion injury (I/R injury) during cardiac arrest and resuscitation is known to turn on the NLRP3 inflammasomes through discrete cell signaling pathways. Inhibition of NLRP3 inflammasome activity improves I/R injury following cardiac arrest in animal models. This minireview discusses the role of the NLRP3 inflammasome in cell damage during cardiac arrest and resuscitation. In addition, the potential application of suppression for NLRP3 activation to improve I/R injury following cardiac arrest and resuscitation is also discussed.

Communication Author：REN Jun , Email:jrenuwyo@ 126.com