Elevated altitudes accompanied by low barometric pressure and acute oxygen deficiency, pose a significant risk for the development of High-Altitude Cerebral Edema in the brain. The resultant HACE is a potentially fatal neurological disorder that triggers a neuroinflammatory response and leads to significant changes in the redox homeostasis of the brain, ultimately resulting in neurodegeneration. In the current study, the level of apoptotic cells and mast cells, as well as the expression of TNF-α as an essential modulator of neuroinflammation was investigated following acute hypobaric hypoxic exposure. The animals were exposed to acute hypobaric hypoxia for approximately 24 h at an altitude of 7620 m. The study findings indicate an increased level of mast cells in the brain parenchyma (p < 0.0001), accompanied by elevated TNF-α expression and TUNEL-positive cells (p < 0.0001), suggestive of neuronal degeneration following acute hypobaric hypoxia. The current study reveals the critical role of mast cells in edema formation during the neuroinflammatory response of the brain under hypoxic conditions. Additionally, it underscores the involvement of pro-inflammatory cytokines, such as TNF-α, in the process of blood brain barrier disruption, and the subsequent development of cerebral edema. This study provides a more in-depth understanding of the pathogenesis of HACE, where the studied biomolecules contribute as essential neuroinflammatory modulators.
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