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Potential mechanisms include activation of the Nrf2-ARE pathway, leading to upregulated expression of endogenous antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase), and suppression of the NF-B pathway, reducing expression of pro-inflammatory cytokines (TNF-, IL-6) and adhesion molecules (VCAM-1, ICAM-1) [2]

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