创伤性脑损伤后脑水肿的病理机制与治疗进展

Pathological mechanism and therapeutic progress of cerebral oedema after traumatic brain injury

创伤性脑损伤(Traumatic Brain Injury,TBI)后脑水肿是继发性颅脑损伤的重要标志,也是不良预后的独立危险因素。目前对TBI的治疗主要集中在稳定患者生命体征和缓解症状上。继发性损伤从原发性损伤后的几小时、几天或几个月陆续出现,包括炎症、脑水肿、血脑屏障(Blood Brain Barrier,BBB)破裂、氧化应激、兴奋性毒性以及线粒体和代谢功能障碍等,继发性损伤极大地影响了患者临床预后。从长期的临床工作来看,在TBI的诸多并发症中,尤以脑水肿(Cerebral Edema,CE)最多见,目前CE的治疗多为非特异性的,如渗透疗法或低温疗法等,对于重度脑水肿临床治疗效果往往不令人满意。因此,了解脑水肿形成的关键分子机制,特别是特异性抗水肿药物的可能靶点,对于对于预防和治疗水肿有重要意义。

Cerebral edema(CE)after traumatic brain injury(TBI)is an important sign of secondary brain injury and an independent risk factor for poor prognosis.At present,the treatment of TBI mainly focuses on stabilizing patients?vital signs and alleviating symptoms.Secondary injury occurs in succession from a few hours,days,or months after the primary injury,including inflammation,CE,blood brain barrier(BBB)rupture,oxidative stress,excitotoxicity,mitochondrial and metabolic dysfunction,etc.Secondary injury greatly affects the clinical prognosis of patients.From the perspective of long-term clinical work,CE is the most common complication of TBI.At present,the treatment of CE is mostly non-specific,such as osmotic therapy or hypothermic therapy,and the clinical treatment effect for severe cerebral edema is often unsatisfactory.Therefore,understanding the key molecular mechanism of CE formation,especially the possible target of specific anti-edema drugs,is of great significance for the prevention and treatment of edema.