International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden.
Department of Chemistry & Biochemistry, University of Arkansas, Fayetteville, AR, United States.
Prog Brain Res. 2020;258:233-283. doi: 10.1016/bs.pbr.2020.09.009. Epub 2020 Oct 24.
Traumatic brain injury (TBI) causes physical injury to the cell membranes of neurons, glial and axons causing the release of several neurochemicals including glutamate and cytokines altering cell-signaling pathways. Upregulation of mitogen associated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) occurs that is largely responsible for cell death. The pharmacological blockade of these pathways results in cell survival. In this review role of several protein kinase inhibitors on TBI induced oxidative stress, blood-brain barrier breakdown, brain edema formation, and resulting brain pathology is discussed in the light of current literature.
创伤性脑损伤（TBI）会导致神经元、神经胶质细胞和轴突的细胞膜物理损伤，导致包括谷氨酸和细胞因子在内的几种神经化学物质释放，改变细胞信号通路。丝裂原激活蛋白激酶（MAPK）和细胞外信号调节激酶（ERK）的上调是细胞死亡的主要原因。这些途径的药理学阻断导致细胞存活。在这篇综述中，根据现有文献，讨论了几种蛋白激酶抑制剂在 TBI 诱导的氧化应激、血脑屏障破坏、脑水肿形成和由此产生的脑病理中的作用。
