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The activation of Nrf2 results in the upregulation of antioxidant gene expression as Nrf2 binds to antioxidant response element (ARE) sites, leading to the expression of key players of the antioxidant response, including heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase 1 (NQO-1), superoxide dismutases (SOD), and glutathione derived molecules catalase, peroxiredoxins, and glutathione peroxidases which collectively attenuate oxidative stress (Khomich et al., 2018

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Long-term dosing studies have also been conducted to evaluate tissue tolerance and inflammation markers, suggesting a favorable profile in terms of local joint impact and systemic safety