儿茶素抑制脑缺血再灌注诱导细胞死亡的研究进展  

Research progress of catechins inhibiting cell death induced by cerebral ischemia/reperfusion

作　　者：沈海英 谢露 陈蒙华[1] SHEN Hai-Ying;XIE Lu;CHEN Meng-Hua(Second Affiliated Hospital of Guangxi Medical University,Nanning 530007,China;Department of Physiology,College of Basic Medical Sciences,Guangxi Medical University,Nanning 530021,China)

机构地区：[1]广西医科大学第二附属医院,南宁530007 [2]广西医科大学基础医学院生理学教研室,南宁530021

出　　处：《生命科学》2024年第2期258-265,共8页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(82160372)。

摘　　要：脑缺血再灌注(ischemic/reperfusion,I/R)最常见于缺血性脑卒中恢复血流再通后以及心脏骤停/心肺复苏(cardiac arrest/cardiopulmonary resuscitation,CA/CPR)后,在再灌注的病理因素条件下引起的脑功能损伤,最终会导致细胞死亡。大量研究表明,脑I/R诱导的细胞死亡形式包括凋亡、焦亡、自噬、坏死性凋亡、铁死亡等,研究细胞死亡可以揭示脑I/R损伤的病理机制,从而为寻找治疗靶点来改善神经功能提供线索。儿茶素作为抗氧化剂能够抑制因氧化应激引起的细胞死亡,而脑I/R诱导细胞死亡的形式存在多样性表明其病理机制具有多样性。因此,本文对其进行归纳总结,旨在揭示其规律,以期能为研究开发治疗脑I/R损伤的药物提供新思路。Cerebral ischemia/reperfusion(I/R)is most commonly observed following the restoration of blood flow after ischemic stroke and during cardiac arrest/cardiopulmonary resuscitation(CA/CPR).Under the pathological conditions of reperfusion,functional damage ultimately results in cell death in the brain.Extensive research has demonstrated that cerebral I/R induces various forms of cell death,including apoptosis,pyroptosis,autophagy,necroptosis,and ferroptosis.Investigating these cell death mechanisms can unveil the underlying pathological processes of cerebral I/R injury,providing valuable insights for identifying therapeutic targets to improve neurological function.Catechins,as antioxidants,have the ability to suppress cell death induced by oxidative stress.The presence of diverse forms of cell death in cerebral I/R highlights the heterogeneous nature of its pathological mechanisms.Therefore,in this review we aim to summarize and identify the patterns of these mechanisms,offering new perspectives for the development of treatments for cerebral I/R injury in both basic and clinical research.

关 键 词：儿茶素 脑缺血再灌注 凋亡 焦亡 自噬 

分 类 号：R743[医药卫生—神经病学与精神病学]