Enriched Environment Ameliorates Cerebral Ischemia-Reperfusion Injury via Dopamine-H₂S Axis-Mediated Dual Mitophagy Activation.

ABSTRACT: Cerebral ischemia-reperfusion injury triggers mitochondrial dysfunction and oxidative stress, exacerbating neuronal apoptosis. Emerging evidence highlights hydrogen sulfide (H₂S) as a gasotransmitter modulating redox balance, autophagy, and apoptosis. This study investigates the neuroprotective mechanisms of Enriched Environment (EE) against ischemic injury, focusing on mitochondrial dynamics and H₂S-mediated pathways. Using MCAO mice and OGD/R-treated SH-SY5Y neurons, interventions targeting H₂S synthesis, hypoxia-inducible factor 1-alpha (HIF-1α), and mitophagy were implemented. Behavioral, histological, and molecular analyses demonstrated EE significantly improved neurological outcomes, suppressed apoptosis, and attenuated oxidative damage (reduced MDA,

SUBMITTER: Zhou B 

PROVIDER: S-EPMC12838293 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature