摘要
急性缺血性脑卒中是由于脑血管堵塞导致局部脑组织血流急剧减少或中断引起的脑组织缺血缺氧性损伤,并出现一系列严重的神经功能缺损症状。黄芪甲苷是我国传统益气中药黄芪的主要有效成分之一,现代药理学研究证明黄芪甲苷对缺血缺氧性脑血管疾病有神经保护作用,可缓解血供恢复后出现的脑缺血再灌注损伤,但其具体作用机制仍有待深入探索。综合近期文献资料,本文就急性缺血性脑卒中的发生机制及黄芪甲苷对脑缺血再灌注损伤的改善作用进行述评,包括改善能量代谢、清除氧自由基、抑制炎症反应、缓解细胞内钙超载、抑制细胞凋亡、保护血脑屏障等,以期为黄芪甲苷作为神经保护药物在脑卒中患者的临床应用提供指导。
Acute ischemic stroke is the ischemic and hypoxic damage of brain tissue caused by the blockage of cerebral blood vessels leading to a sharp decrease or interruption of local brain tissue blood flow,and a series of severe neurological deficit symptoms.Astragaloside Ⅳ is one of the main effective components of Astragalus,a traditional Chinese medicine for replenishing Qi.Modern pharmacological studies have proved that Astragaloside Ⅳ has an obvious neuroprotective effect on hypoxic-ischemic cerebrovascular disease and can relieve cerebral ischemia reperfusion injury after blood supply is restored.But its specific mechanism remains to be further explored.Based on recent literature data,this article reviews the mechanism of Acute ischemic stroke and the improvement effect of Astragaloside Ⅳ on cerebral ischemia-reperfusion,including improving energy metabolism,eliminating oxygen free radicals,inhibiting inflammation,and relieving intracellular Calcium overload,inhibition of cell apoptosis,protection of the blood-brain barrier,etc.,in order to provide guidance for the clinical application of Asragaloside Ⅳ as a neuroprotective drug in stroke patients.
作者
杜澍金
高维娟
DU Shu-jin;GAO Wei-juan(Hebei Key Laboratory of Chinese Medicine Research on Cardio-cerebrovascular Disease,Hebei University of Chinese Medicine,Shijiazhuang 050200,China)
出处
《中国中医基础医学杂志》
CAS
CSCD
北大核心
2021年第9期1532-1532,F0003,F0004,共3页
JOURNAL OF BASIC CHINESE MEDICINE
基金
河北中医学院青年教师科研能力提升项目(YJZ2019004)-黄芪甲苷对脑缺血再灌注后海马神经细胞凋亡的影响及作用机制研究
河北中医学院优秀青年教师基础研究项目(YQ2019007)-黄芪甲苷通过钙敏感受体调控钙超载抑制脑缺血再灌注损伤的机制研究
河北省中西医结合肝肾病证研究重点实验室开放课题(B201903)-脑缺血再灌注致肾损伤的作用机制及化瘀解毒中药的保护作用。
关键词
黄芪甲苷
急性缺血性脑卒中
脑缺血再灌注损伤
保护
凋亡
AstragalosideⅣ
Acute ischemic stroke
Cerebral ischemia-reperfusion injury
Protection
Apoptosis
