Cortical neuronal cell death following traumatic brain injury (TBI) evoked by the cortical impact is a significant factor that contributes to neurological deficits. In the current study, we harvested the injured area and perilesional area of the injured brain induced by TBI. We explored the functions of Sec22b, an apoptosis-promoting kinase, and a pivotal bridge builder of apoptotic signaling in the etiopathogenesis of an experimental rat model of TBI. We found that Sec22b was expressed in neurons in the injured cortical area, and the expression level significantly decreased after TBI, especially at 24 h. Administration of Sec22b overexpressed plasmid significantly ameliorated TBI-induced apoptosis, neurological deficits, and blood-brain barrier permeability, accompanied by the activation of autophagy. However, the administration of Sec22b knockdown resulted in the opposite eff ;ects. Altogether, these findings indicated that Sec22b plays a neuroprotective role after TBI, suggesting that Sec22b may be a potential therapeutic target for TBI. We speculated that this neuroprotective effect might be achieved by upregulating autophagy levels and required further studies to explore.

由皮质撞击引起的外伤性脑损伤 (TBI) 后皮质神经元细胞死亡是导致神经功能障碍的重要因素。在目前的研究中，我们收获了 TBI 诱导的受伤大脑的受伤区域和周围区域。我们探讨了 Sec22b、一种凋亡促进激酶和 TBI 实验大鼠模型的发病机制中凋亡信号传导的关键桥梁建设者的功能。我们发现 Sec22b 在受损皮层区域的神经元中表达，并且在 TBI 后表达水平显着降低，尤其是在 24 h 时。施用 Sec22b 过表达的质粒显着改善了 TBI 诱导的细胞凋亡、神经系统缺陷和血脑屏障通透性，同时激活了自噬。然而，Sec22b 敲低的管理导致了相反的效果。总之，这些发现表明 Sec22b 在 TBI 后发挥神经保护作用，表明 Sec22b 可能是 TBI 的潜在治疗靶点。我们推测这种神经保护作用可能是通过上调自噬水平来实现的，需要进一步的研究来探索。