The International journal of neuroscience · 2026
Astaxanthin alleviates ischemia-reperfusion injury by regulating the JAK2/STAT3 signaling pathway.
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Zhang Yuhong, Jiang Jingxi, Ma Zhenhuan, Gong Hong
Аннотация
BACKGROUND: Cerebral ischemia-reperfusion injury (CIRI) lacks effective treatments. Astaxanthin (AST) ameliorates CIRI, but the underlying mechanisms remain unclear.
METHODS: An oxygen-glucose deprivation/reoxygenation (OGD/R) model in PC12 cells and a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model were used. Cell viability (MTT), apoptosis (flow cytometry), oxidative damage (8-OHdG, 4-HNE, MDA, ROS), inflammatory factors (TNF-α, IL-1β, IL-6, MCP-1), and JAK2/STAT3 pathway proteins (p-JAK2, p-STAT3) were assessed, with or without AST treatment and JAK2 agonist intervention.
RESULTS: OGD/R significantly reduced PC12 cell viability, increased apoptosis, and elevated oxidative and inflammatory markers, while activating JAK2/STAT3. AST treatment reversed these effects-promoting proliferation, inhibiting apoptosis, and reducing damage markers. AST also suppressed p-JAK2 and p-STAT3 expression. Activation of the JAK2/STAT3 pathway abolished AST's protective effects against OGD/R-induced damage. In vivo, AST effectively alleviated ischemia-reperfusion injury in rats.
METHODS: An oxygen-glucose deprivation/reoxygenation (OGD/R) model in PC12 cells and a middle cerebral artery occlusion/reperfusion (MCAO/R) rat model were used. Cell viability (MTT), apoptosis (flow cytometry), oxidative damage (8-OHdG, 4-HNE, MDA, ROS), inflammatory factors (TNF-α, IL-1β, IL-6, MCP-1), and JAK2/STAT3 pathway proteins (p-JAK2, p-STAT3) were assessed, with or without AST treatment and JAK2 agonist intervention.
RESULTS: OGD/R significantly reduced PC12 cell viability, increased apoptosis, and elevated oxidative and inflammatory markers, while activating JAK2/STAT3. AST treatment reversed these effects-promoting proliferation, inhibiting apoptosis, and reducing damage markers. AST also suppressed p-JAK2 and p-STAT3 expression. Activation of the JAK2/STAT3 pathway abolished AST's protective effects against OGD/R-induced damage. In vivo, AST effectively alleviated ischemia-reperfusion injury in rats.