Abstract：
High-altitude environments present extreme conditions characterized by low barometric pressure and oxygen deficiency, which can disrupt brain functioning and cause edema formation. The objective of the present study is to investigate several biomolecule expressions and their role in the development of High Altitude Cerebral Edema in a rat model. Specifically, the study focuses on analyzing the changes in total arginase, nitric oxide, and lipid peroxidation (MDA) levels in the brain following acute hypobaric hypoxic exposure (7620 m, SO2=8.1 %, for 24 h) along with the histopathological assessment. The histological examination revealed increased TNF-α activity, and an elevated number of mast cells in the brain, mainly in the hippocampus and cerebral cortex. The research findings demonstrated that acute hypobaric hypoxic causes increased levels of apoptotic cells, shrinkage, and swelling of neurons, accompanied by the formation of protein aggregation in the brain parenchyma. Additionally, the level of nitric oxide and MDA was found to have increased (p<0.0001), however, the level of arginase decreased indicating active lipid peroxidation and redox imbalance in the brain. This study provides insights into the pathogenesis of HACE by evaluating some biomolecules that play a pivotal role in the inflammatory response and the redox landscape in the brain. The findings could have significant implications for understanding the neuronal dysfunction and the pathological mechanisms underlying HACE development.
摘要：
高海拔环境呈现以低气压和缺氧为特征的极端条件，这会破坏大脑功能并导致水肿形成。本研究的目的是研究几种生物分子的表达及其在大鼠模型高原脑水肿发展中的作用。具体来说,这项研究的重点是分析总精氨酸酶的变化，一氧化氮,和急性低压低氧暴露后大脑中的脂质过氧化（MDA）水平（7620m，SO2=8.1%，24小时）以及组织病理学评估。组织学检查显示TNF-α活性增加，大脑中肥大细胞数量增加，主要在海马和大脑皮层.研究结果表明，急性低压低氧会导致凋亡细胞水平升高，收缩，和神经元的肿胀，伴随着脑实质中蛋白质聚集的形成。此外,发现一氧化氮和丙二醛的水平增加（p<0.0001），然而,精氨酸酶水平降低，表明大脑中活性脂质过氧化和氧化还原失衡。这项研究通过评估一些在炎症反应和大脑氧化还原景观中起关键作用的生物分子，为HACE的发病机理提供了见解。该发现可能对理解神经元功能障碍和HACE发展的病理机制具有重要意义。
