ArticleNeurochemical research2025
Phylloquinone Attenuates Oxygen-Glucose Deprivation-induced Neuronal Injury by Inhibiting Ferroptosis via the xCT/GPX4 Pathway.
Article in Neurochemical research, 2025. 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
Neuronal cell damage resulting from ischemic and hypoxic injury is a major pathological event in stroke, with ferroptosis increasingly recognized as a contributing mechanism. In this study, we observed that oxygen-glucose deprivation (OGD) triggered ferroptosis in neuronal cells. By screening of naphthoquinone compounds intervening oxidative stress, we have identified phylloquinone (VK1, also known as vitamin K1) as a potent inhibitor of ferroptosis with significant neuroprotective effects. Phylloquinone also alleviated OGD-induced cellular senescence. Mechanistic investigation revealed that Kruppel-like factor 2 (Klf2) is a potential target of phylloquinone and participates in its neuroprotective effects. These findings indicate that phylloquinone protects neurons from OGD-induced injury by inhibiting ferroptosis through the xCT/GPX4 pathway, highlighting its potential as a therapeutic candidate for ischemic neuronal damage.
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