ArticleExperimental brain research2026
Dexmedetomidine inhibits microglia ferroptosis to relieve postoperative cognitive dysfunction in elderly rats through JPX/HIF-1/DHODH pathway.
Article in Experimental brain research, 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
backgroundPostoperative cognitive dysfunction (POCD) is a prevalent neurological consequence in aged patients, with neuroinflammation and ferroptosis implicated in its pathogenesis. This study investigates whether dexmedetomidine (DEX) alleviates POCD by modulating the JPX/HIF-1α/DHODH axis.
methodAged Sprague-Dawley rats received excision of the right common carotid artery to establish POCD. DEX (12 μg/kg) was administered preoperatively. Cognitive performance was evaluated through behavioral paradigms including spatial navigation tasks (Morris water maze) and recognition memory assessments (novel object test). Hippocampal ferroptosis markers (Fe
resultDEX ameliorated cognitive deficits and suppressed hippocampal ferroptosis. Mechanistically, JPX recruits HIF-1α to transcriptionally activate DHODH expression, while DEX upregulated JPX to facilitate HIF-1α-mediated DHODH transcription. In BV-2 cells, DEX attenuated LPS-induced ferroptosis, whereas JPX silencing abolished its effects. DHODH overexpression counteracted siJPX's exacerbation of ferroptosis.
conclusionDEX alleviates POCD by inhibiting microglial ferroptosis via the JPX/HIF-1α/DHODH axis, providing a novel therapeutic target for POCD intervention.
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