ArticleMolecular neurobiology2026
Dendrobium Officinale Polysaccharide Inhibits Ferroptosis and Ameliorates Cerebral Ischemia-Reperfusion Injury: Involvement of the Nrf2/GPX4 Signaling Pathway.
Article in Molecular neurobiology, 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
Ferroptosis, a critical pathological mechanism in ischemic stroke (IS), is activated during the early phase of cerebral ischemia-reperfusion injury (CI/RI). Dendrobium officinale polysaccharide (DOP), the primary bioactive component of Dendrobium officinale, exhibits diverse pharmacological activities, including antioxidant, anti-inflammatory, and immunomodulatory effects. DOP has been suggested to exert neuroprotective effects by inhibiting ferroptosis; however, its specific role and underlying mechanisms in IS-related ferroptosis remain unclear. In this study, in vivo and in vitro CI/RI models were established using middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R), respectively. DOP was administered under a paradigm combining long-term pretreatment and short-term post-ischemic intervention, and its neuroprotective effects were evaluated. In MCAO/R mice, DOP significantly alleviated neurological deficits, reduced the cerebral infarct volume, and mitigated neuronal damage. These effects were associated with decreased Fe
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