创伤性脑损伤后尿酸通过抗氧化应激促进神经损伤修复的作用及可能机制

The role and possible mechanism of uric acid in promoting nerve injury repair through anti-oxidative stress after traumatic brain injury

创伤性脑损伤(TBI)致死率、致残率高,是严重危害国人健康的公共卫生问题之一。TBI后病理损伤可分为原发性损伤和继发性损伤。控制原发性损伤的有效治疗主要依靠手术。然而,各种病理机制导致继发性损伤,导致神经细胞丢失。氧化应激是继发性损伤进展过程中常见的病理现象之一。因此,探索减轻氧化应激的途径可能是减轻脑外伤后继发性损伤,并促进神经再生的有效干预手段。尿酸(UA)作为体内抗氧化剂之一,不仅通过抗氧化应激起保护神经作用,同时还可能激活神经干细胞增殖参与损伤修复,提高患者神经功能恢复。现就尿酸在TBI继发性损伤中的作用及可能的机制作一初步的阐述,其目的是扩大UA在TBI治疗中的应用。

Traumatic brain injury(TBI)has been becoming one of the leading public health problems as a result of its high mortality and disability rate.Targeting the pathophysiological mechanism of TBI is a pivotal link to develop therapeutic methods to promote neurological rehabilitation of TBI patients.The category of pathologic injury post-TBI could be divided into primary damage and secondary injury.The effective treatment for controlling primary damage mainly relies on surgery.While,various pathologic mechanisms cause secondary injury that results in loss of neural cells.Oxidative stress is one of the common pathologic phenomena during the progression of secondary injury.Therefore,exploring approaches aiming to mitigate oxidative stress might be an effective intervention relieving secondary injury to promote neuroregeneration after TBI.Uric acid(UA),one of the in vivo antioxidants,not only exerts neuroprotection through alleviating oxidative stress,but also might possess the ability of promoting the proliferation of neural stem cell(NSC)that participates in neural repair after TBI,thereafter improving the neurological recovery.Here,we preliminarily reviewed the effect of UA on secondary injury of post-TBI and the possible underlying mechanisms.The aim of this review was to broaden the use of UA in the treatment of TBI.