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30 min pretreatment, followed by 24 h AβO exposure) dose-dependently inhibits the release of proinflammatory mediators (TNF-α, IL-1β, NO) induced by AβO in primary mouse microglia, suppresses oxidative stress, and restores the antioxidant capacity of cells [5]
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Cystine is reduced to cysteine, which is a rate-limiting precursor in glutathione synthesis
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