摘要
创伤性脑损伤(TBI)是由交通事故、跌倒等造成的一种复杂的头部获得性直接损伤,包括原发性脑损伤和继发性脑损伤,其中继发性脑损伤(sTBI)产生的二级生化级联反应(如氧化应激反应、炎症反应、谷氨酸神经毒性反应)是导致神经功能障碍的最主要原因。红景天苷(Sal)是从红景天根茎中分离出的一种天然酚类产物,具有抗氧化、抑制炎症和凋亡、阻断神经传递等神经保护作用。因其在神经保护中疗效显著,且副反应少,已成为治疗TBI后继发性脑损伤药物中的研究热点。虽然临床上关于sTBI的治疗已有广泛研究,但目前仍缺乏Sal改善sTBI所致神经功能障碍的机制总结,因此本文就Sal改善TBI后继发神经功能障碍的最新研究进展及作用机制作一综述,以期为临床上应用Sal改善此类疾病及其并发症提供参考。
Traumatic brain injury(TBI) is a complex direct injury to the head caused by traffic accidents,falls,etc.,including primary brain injury and secondary brain injury.Secondary biochemical cascade reactions(such as oxidative stress,inflammation and glutamate neurotoxicity) generated by Secondary traumatic brain injury(sTBI) are the main causes of neurological dysfunction.Salidroside(Sal) is a natural phenolic product isolated from Rhodiola rosea Rhizome,which has neuroprotective effects such as anti-oxidation,inhibiting inflammation and apoptosis,blocking neurotransmission and so on.Because of its remarkable effect in neuroprotection and few side effects,it has become a research hotspot in the treatment of secondary brain injury after TBI.Although there have been extensive clinical studies on the treatment of sTBI,there is still no summary of the mechanism by which Sal can improve the neurological dysfunction caused by sTBI.Therefore,this paper summarizes the latest research progress and mechanism of action of Sal in improving the secondary neurological dysfunction of TBI,in order to provide references for the clinical application of Sal to improve such diseases and their complications.
作者
陈琳
葛红飞
喻安永
Chen Lin;Ge Hongfei;Yu Anyong(Department of Emergency,Affiliated Hospital of Zunyi Medical University,Zunyi Guizhou 563003,China;Department of Neurosurgery,the First Affiliated Hospital of Army Medical University,Chongqing 400037,China)
出处
《遵义医科大学学报》
2024年第4期416-423,共8页
Journal of Zunyi Medical University
基金
国家自然科学基金资助项目(NO:82060245)
省部共建协同创新中心项目[NO:教科技厅函(2020)39]。
关键词
创伤性脑损伤
继发性脑损伤
红景天苷
氧化应激反应
炎症反应
谷氨酸兴奋性神经毒性反应
traumatic brain injury
secondary traumatic brain injury
salidroside
oxidative stress reaction
inflammatory response
glutamate excitatory neurotoxic reaction
