首页|儿茶素抑制脑缺血再灌注诱导细胞死亡的研究进展

儿茶素抑制脑缺血再灌注诱导细胞死亡的研究进展

扫码查看
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.
Research progress of catechins inhibiting cell death induced by cerebral ischemia/reperfusion
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.

catechinscerebral ischemia/reperfusionapoptosispyroptosisautophagy

沈海英、谢露、陈蒙华

展开 >

广西医科大学第二附属医院,南宁 530007

广西医科大学基础医学院生理学教研室,南宁 530021

儿茶素 脑缺血再灌注 凋亡 焦亡 自噬

国家自然科学基金项目

82160372

2024

生命科学
国家自然科学基金委员会生命科学部 中国科学院生命科学与生物技术局 中国科学院生命科学和医学学部 中国科学院上海生命科学研究院

生命科学

CSTPCD
影响因子:0.542
ISSN:1004-0374
年,卷(期):2024.36(2)
  • 79