Wang Zeqian, Duan Yanzhe, Wu Yige, Ma Cungen, Yan Yuqing, Song Lijuan
Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619; Shanxi Key Laboratory of Inflammatory Neurodegenerative Diseases, Institute of Brain Science, Shanxi Datong University, Datong 037009, China. *Corresponding authors, E-mail:
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2024 Jul;40(7):648-654.
Ischemic stroke is one of the diseases which pose a significant threat to human health. Recent studies have suggested that programmed cell death plays an important role in brain tissues affected by ischemia and hypoxia. Pyroptosis, which is characterized by both apoptosis and necrosis, is mediated by activation of inflammasomes, such as NOD-like receptor family, pyrin domain containing 3 (NLRP3). Pyroptosis, which depends on caspase-1 activation and the release of pro-inflammatory cytokines, such as Interleukin 1β and Interleukin 18, plays a vital role in regulating cell survival and death following ischemic injury. Previous studies have shown that pyroptosis is closely related to the activation of the NLRP3 inflammasome in ischemic stroke tissues. This distinctive form of cell death mainly occurs in microglia, neurons, astrocytes and endothelial cells. This paper reviews the role of pyroptosis mediated by inflammasomes in ischemic stroke, discussing the targets and substances that affect the activation of the NLRP3 inflammasome, which can provide a new theoretical and experimental basis for the treatment of ischemic stroke.
缺血性中风是对人类健康构成重大威胁的疾病之一。最近的研究表明，程序性细胞死亡在受缺血和缺氧影响的脑组织中起重要作用。以凋亡和坏死为特征的细胞焦亡由炎性小体激活介导，如含NOD样受体家族吡咯结构域3（NLRP3）。细胞焦亡依赖于半胱天冬酶-1的激活以及促炎细胞因子如白细胞介素1β和白细胞介素18的释放，在调节缺血性损伤后的细胞存活和死亡中起重要作用。先前的研究表明，细胞焦亡与缺血性中风组织中NLRP3炎性小体的激活密切相关。这种独特的细胞死亡形式主要发生在小胶质细胞、神经元、星形胶质细胞和内皮细胞中。本文综述了炎性小体介导的细胞焦亡在缺血性中风中的作用，探讨了影响NLRP3炎性小体激活的靶点和物质，可为缺血性中风的治疗提供新的理论和实验依据。
