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创伤性脑损伤(traumatic braininjury,TBI)后的继发脑损伤出现在原发伤后的数小时到数天,是各种细胞、生化介质构成级联网络反应的结果,继而导致了颅内压升高、脑缺血、脑水肿等。TBI后的炎症反应是TBI后病理进程的重要组成部分,是导致TBI后继发脑损伤的主导因素,近年的研究已逐步认识了TBI后炎症反应中所参与的细胞、涉及的细胞因子、可能存在的上游调控蛋白,并提出TBI后炎症反应与神经元凋亡、脑组织水肿及血脑屏障破坏有密切关系。本文对TBI后炎症反应的相关研究作一简述,主要包括TBI后炎症反应的发生,TBI后炎症反应与脑水肿、神经元凋亡的关系,以及主要参与TBI后炎症反应的细胞因子及相关调控蛋白质。
Secondary traumatic brain injury (traumatic brain injury, traumatic brain injury, TBI) occurred in a few hours after the primary injury to several days, is a variety of cells, biochemical mediators constitute a cascade of network results, which led to intracranial pressure Elevated, cerebral ischemia, cerebral edema and so on. Inflammatory reaction after TBI is an important part of the pathological process after TBI and is the leading factor leading to secondary brain injury after TBI. In recent years, studies have gradually recognized the cells involved in the inflammatory response after TBI, the cytokines involved may exist Of the upstream regulatory proteins, and proposed inflammatory response after TBI and neuronal apoptosis, brain tissue edema and blood-brain barrier damage are closely related. In this article, the related research on inflammatory reaction after TBI is briefly summarized, including the occurrence of inflammatory reaction after TBI, the relationship between inflammatory reaction and cerebral edema and neuron apoptosis after TBI, and the cytokines and their correlation mainly involved in inflammation after TBI Regulate proteins.