摘要
创伤性脑损伤合并海水浸泡(TBI+SI)是现代海战、海上作业的常见病,致死致残率高。由于损伤机制复杂,其临床救治是一个棘手的问题。神经炎症诱发的细胞焦亡是TBI+SI的一个重要损伤机制,它加剧了神经元死亡,导致患者的不良预后。因此,针对细胞焦亡的干预或许可以成为有效的治疗手段。基于各种研究结果,本文提出新假说:神经调节蛋白-1(Nrg-1)通过激活其受体ErbB,可以抑制TLR4/NF-κB/NLRP3信号通路,减少神经炎性反应,进而抑制细胞焦亡,从而达到缓解TBI+SI损伤的效果。此假说若被证明,可以为TBI+SI的临床辅助治疗提供新的方向,改善患者的预后。
Traumatic brain injury combined with seawater immersion(TBI+SI)is a common disease in modern naval warfare and offshore operations,with a high fatality and disability rate.Due to the complexity of the injury mechanism,its clinical treatment remains a tricky problem.Pyroptosis induced by neuroinflammation is an important injury mechanism of TBI+SI,which exacerbates neuronal death and leads to poor prognosis of patients.Therefore,intervention against pyroptosis may be an effective treatment strategy.Based on various research results,this article proposes a hypothesis that nerve growth factor Nrg-1 can inhibit the TLR4/NF-κB/NLRP3 signaling pathway by activating its receptor ErbB,reducing neuroinflammatory reactions,and thereby inhibiting pyroptosis,and hence alleviating TBI+SI injury.If this hypothesis is proven,it can provide a new direction for clinical adjunctive therapy of TBI+SI and improve the prognosis of patients.
作者
杨洋
陈力
徐永君
王守森
YANG Yang;CHEN Li;XU Yongjun;WANG Shousen(Department of Neurosurgery,Fu Zong Teaching Medical College(Hospital No.900),Fujian University of Traditional Chinese Medicine,Fuzhou,Fujian 350025,China;Department of Neurosurgery,Fu Zong Clinical Medical College(Hospital No.900),Fujian University of Traditional Chinese Medicine,Fuzhou,Fujian 350025,China)
出处
《中华神经外科疾病研究杂志》
2025年第3期174-177,共4页
Chinese Journal of Neurosurgical Disease Research
基金
联勤医学重点专科(神经外科)项目(LQZD-SW)
福建省科技计划科技创新平台项目(2022Y2017)。
