The slightly available data about the pathogenesis process of mild repetitive traumatic brain injury (mRTBI) indicates to the necessity of further exploration of mRTBI consequences. Several cellular changes are believed to contribute to the cognitive disabilities, and neurodegenerative changes observed later in persons subjected to mRTBI. We investigated glial fibrillary acidic protein (GFAP), the important severity related biomarker, where it showed further increase after multiple trauma compared to single one. To authenticate our aim, Morin (10 mg/kg loading dose, then twice daily 5 mg/kg for 7 days), MK-801 (1 mg/kg; i.p) and their combination were used. The results obtained has shown that all the chosen regimens opposed the upregulated dementia markers (Aβ1-40,p(Thr231)Tau) and inflammatory protein contents/expression of p(Ser53s6)NF-κBp65, TNF-α, IL-6,and IL-1β and the elevated GFAP in immune stained cortex sections. Additionally, they exerted anti-apoptotic activity by decreasing caspase-3 activity and increasing Bcl-2 contents. Saving brain tissues was evident after these therapeutic agents via upregulating the non-canonical Wnt-1/PKC-α cue and IL-10/p(Tyr(1007/1008))JAK-2/p(Tyr705)STAT-3 signaling pathway to confirm enhancement of survival pathways on the molecular level. Such results were imitated by correcting the injury dependent deviated behavior, where Morin alone or in combination enhanced behavior outcome. On one side, our study refers to the implication of two survival signaling pathways; viz.,the non-canonical Wnt-1/PKC-α and p(Tyr(1007/1008))JAK-2/p(Tyr705)STAT-3 in single and repetitive mRTBI along with distorted dementia markers, inflammation and apoptotic process that finally disrupted behavior. On the other side, intervention through affecting all these targets by Morin alone or with MK-801 affords a promising neuroprotective effect.

关于轻度重复性创伤性脑损伤 (mRTBI) 发病机制过程的少量可用数据表明有必要进一步探索 mRTBI 后果。一些细胞变化被认为会导致认知障碍，以及后来在接受 mRTBI 的人中观察到的神经退行性变化。我们研究了胶质纤维酸性蛋白 (GFAP)，这是一种重要的严重程度相关生物标志物，与单一创伤相比，它在多次创伤后显示出进一步增加。为了验证我们的目标，使用了 Morin（10 mg/kg 负荷剂量，然后每天两次 5 mg/kg，持续 7 天）、MK-801（1 mg/kg；ip）及其组合。获得的结果表明，所有选择的方案都反对上调的痴呆标志物（Aβ1-40，p(Thr231)Tau) 和炎症蛋白含量/ p (Ser53s6)NF-κBp65、TNF-α、IL-6 和 IL-1β 的表达以及免疫染色皮质切片中升高的 GFAP。此外，它们通过降低 caspase-3 活性和增加 Bcl-2 含量来发挥抗凋亡活性。通过上调非经典 Wnt-1/PKC-α 信号和 IL-10/ p (Tyr(1007/1008))JAK-2/ p (Tyr705)STAT-3 信号通路，这些治疗剂明显挽救脑组织在分子水平上确认生存途径的增强。通过纠正损伤依赖的偏差行为来模仿这些结果，其中 Morin 单独或组合增强了行为结果。一方面，我们的研究涉及两种生存信号通路的含义；即，非经典 Wnt-1/PKC-α 和p (Tyr(1007/1008))JAK-2/ p (Tyr705)STAT-3 在单一和重复 mRTBI 以及扭曲的痴呆标志物、炎症和凋亡过程最终打乱了行为。另一方面，通过单独使用 Morin 或与 MK-801 影响所有这些目标进行干预，可提供有希望的神经保护作用。