乙酰唑胺在急性低氧暴露中的神经保护作用机制进展OA

Acute hypoxic exposure can induce functional brain impairment,driven by molecular mechanisms including mitochondrial dysfunction,intracellular calcium overload,glial cell activa-tion and inflammatory responses,blood-brain barrier disruption,and alterated cerebral blood flow.Acetazolamide,a broad-spectrum carbonic anhydrase inhibitor,is a standard clinical treat-ment and remains the only medication approved by the Food and Drug Administration for the prevention and treatment of acute mountain sickness.Substantial evidence confirms that under acute hypoxic exposure,acetazolamide exerts multi-level neuroprotective effects on brain tissue by inhibiting carbonic anhydrase VB and other isoforms.These protective mechanisms involve preserving mitochondrial integrity,regulating calcium homeostasis and pH balance,modulating glial cell activity to mitigate neuroinflammation,maintaining blood-brain barrier structure in-tegrity,and improving cerebral perfusion through cerebrovascular regulation.This article reviewed the molecular pathological mechanisms of hypoxia-induced nervous system damage,summarized the pharmacological properties and neuroprotective effects of acetazolamide,and provided a theoretical basis for therapeutic interventions against high-altitude hypoxic neural injury.