ArticleFrontiers in pharmacology2026
Carnosic acid alleviates high-altitude cerebral edema by suppressing oxidative stress and microglia activation-induced neuroinflammation.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Oxidative stress and neuroinflammation constitute key pathological contributors to high-altitude cerebral edema (HACE). Carnosic acid (CA) exerts important roles in neurodegeneration and brain injury, but its function in HACE remains elusive. Methods: High-altitude hypobaric hypoxic (HH)-mimicked HACE rats were administered carnosic acid. The effects on hematological parameter changes, blood-brain barrier (BBB) permeability, energetic metabolism disorder, cognitive and motor impairment, oxidative stress, and microglia-mediated neuroinflammation were explored. The function of carnosic acid in microglia-mediated damage to astrocytes and endothelial cells under hypoxia was investigated. Results: Carnosic acid dose-dependently normalized aberrant hematological parameter changes, brain water content, and histopathological changes in HH-mimicked HACE rats. Moreover, HH conditions enhanced BBB permeability and BBB-related aquaporin 4 (AQP4) expression and decreased BBB-related occludin and zonula occludens-1 (ZO-1) expression, which were reversed after carnosic acid. Carnosic acid alleviated energetic metabolism disorder and improved cognitive and motor impairment in HACE rats. Carnosic acid attenuated HH-evoked oxidative stress by inhibiting reactive oxygen species (ROS) and malondialdehyde levels and increased antioxidant glutathione and superoxide dismutase levels. Carnosic acid suppressed HH-induced microglia activation and pro-inflammatory response. Additionally, aberrant activation of the NF-κB-NLRP3 inflammasome axis in HACE rats was also inhibited by carnosic acid. Carnosic acid inhibited hypoxia-induced pro-inflammatory microglia activation by the NF-κB-NLRP3 pathway. Moreover, carnosic acid also attenuated hypoxia-activated microglia-induced AQP4 expression in astrocytes and damage to the endothelial tight junction. Conclusion: Carnosic acid may attenuate the pathological progression of HACE by restraining oxidative stress and microglia activation-induced neuroinflammation via the NF-κB-NLRP3 axis, supporting it as a promising neuroprotective intervention for HACE.
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