Khan Rifat Ullah, Jawad Sahibzada Muhammad, Kiyani Mubin Mustafa, Shah Shahid Ali, Bashir Shahid, Khan Hamid
Department of Chemical and Life Sciences, Qurtuba University of Science and Information Technology, Peshawar, KP, Pakistan.
Department of Zoology Islamia College University Peshawar, KP, Pakistan.
Heliyon. 2024 Sep 18;10(18):e38106. doi: 10.1016/j.heliyon.2024.e38106. eCollection 2024 Sep 30.
Traumatic brain injury (TBI) is an increasing widespread cause of disability and mortality, typically leading to dementia and memory impairment.
This study aims to investigate the neuroprotective potential of extract against TBI induced memory impairment in adult albino mice.
Adult male mice were divided into four groups randomly: Control, extract alone, TBI alone and TBI plus extract. TBI induction was carried out in mice using a weight dropping method then extract (10 mg/kg) was administered intraperitoneally for two weeks. Morris water maze and Y-maze tests were used to measure memory improvement ability and Western blot technique was used to analyse the neuroinflammatory and synaptic protein markers.
extract significantly decreased phosphorylated c-Jun N-terminal kinase (p-JNK), Tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa B (NF-κB) proteins to reduce TBI-induced neuroinflammation accompanied by the restoration of both pre- and post-synaptic protein expression in adult mice model. Furthermore, extract enhanced both short and long-term spatial memory against TBI in adult mice model.
extract abrogated neuroinflammation mediated memory impairment in TBI mice model. Further research is needed to determine extract ingredients detail completely and to understand its mechanisms of neuroprotection in reducing memory impairments associated with traumatic brain injury and other neurodegenerative diseases.
创伤性脑损伤（TBI）是导致残疾和死亡的一个日益普遍的原因，通常会导致痴呆和记忆障碍。
本研究旨在探讨提取物对成年白化病小鼠TBI诱导的记忆障碍的神经保护潜力。
将成年雄性小鼠随机分为四组：对照组、单独给予提取物组、单独TBI组和TBI加提取物组。采用重物坠落法对小鼠进行TBI诱导，然后腹腔注射提取物（10mg/kg），持续两周。采用Morris水迷宫和Y迷宫试验测量记忆改善能力，采用蛋白质免疫印迹技术分析神经炎症和突触蛋白标志物。
提取物显著降低磷酸化c-Jun氨基末端激酶（p-JNK）、肿瘤坏死因子-α（TNF-α）和核因子κB（NF-κB）蛋白水平，以减轻TBI诱导的神经炎症，同时恢复成年小鼠模型中突触前和突触后蛋白的表达。此外，提取物增强了成年小鼠模型中针对TBI的短期和长期空间记忆。
提取物消除了TBI小鼠模型中神经炎症介导的记忆障碍。需要进一步研究以完全确定提取物的成分细节，并了解其在减少与创伤性脑损伤和其他神经退行性疾病相关的记忆障碍中的神经保护机制。
