摘要
缺血性卒中是全球死亡和致残的主要原因,恢复脑组织的血流量(再灌注)是目前最有效的治疗方法。然而,再灌注后,脑组织中过量活性氧的产生,炎症细胞异常募集,炎症因子过量释放,细胞自噬,线粒体功能障碍,钙稳态失调,内质网应激,谷氨酸兴奋性毒性,细胞凋亡及血脑屏障破坏等病理机制会进一步加重细胞损伤和死亡,最终影响神经功能恢复。大量的研究表明姜黄素可通过抑制脑缺血再灌注损伤的多种病理机制而发挥显著神经保护作用,最终改善脑循环,减少梗死体积,减少脑水肿,促进血脑屏障修复,改善神经功能。因此,姜黄素可通过减轻脑缺血再灌注损伤而改善神经功能,具有补充现有缺血性卒中治疗方法的潜力。
Ischemic stroke is a major cause of death and disability in the world.Currently,the most effective treatment for ischemic stroke is to prevent ischemia and hypoxia injury and repair damaged tissues by restoring blood flow(reperfusion).Although reperfusion is a signal for the termination of ischemia and hypoxia,it may subsequently increase cell damage and death through excessive production of reactive oxygen species,abnormal recruitment of inflammatory cells,and excessive release of inflammatory factors,autophagy,mitochondrial dysfunction,calcium homeostasis disorder,endoplasmic reticulum stress,glutamate excitotoxicity,apoptosis,destruction of blood-brain barrier and other mechanisms.A large number of studies have shown that curcumin can play a significant neuroprotective effect by slowing down various pathological mechanisms of ischemia-reperfusion injury,and ultimately improving cerebral circulation,reducing infarct volume,reducing cerebral edema,promoting blood-brain barrier repair,and improving neurological function.Therefore,curcumin can improve neurological function by alleviating ischemia-reperfusion injury,and has the potential to supplement the existing treatment methods for ischemic stroke.
作者
刘小艳
田野
刘骥飞
苏刚
张振昶
LIU Xiaoyan;TIAN Ye;LIU Jifei;SU Gang;ZHANG Zhenchang(Lanzhou University Second Clinical Medical College, Lanzhou 730000, Gansu, China;Institute of Genetics, Lanzhou University School of Basic Medical Sciences, Lanzhou 730000, Gansu, China;Department of Neurology, Lanzhou University Second Hospital, Lanzhou 730030, Gansu, China)
出处
《中国临床药理学与治疗学》
CAS
CSCD
2019年第11期1305-1309,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
国家自然科学基金面上项目(31870335)
关键词
姜黄素
脑缺血再灌注损伤
神经保护
curcumin
cerebral ischemia-reperfusion injury
neuroprotection