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. 2021 Oct 22;22(6):1473. doi: 10.3892/etm.2021.10908

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Copyright: © Li et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Molecular mechanism of TPs protection against H₂O₂-induced RAW264.7 cell injury. The excessive production of ROS in H₂O₂-injured RAW264.7 cells is alleviated and the balance of the oxidoreductase system is maintained by TPs. The expression of Nrf2 is directly affected by the change of intracellular ROS levels, following the Mst/Nrf2 axis maintenance of cellular redox balance and via Nrf2 binding to the ARE in the nucleus and thereby activating HO-1 protein expression. Induction via the Mst/Nrf2 axis and the Keap1/Nrf2/HO-1 pathway appears to represent the antioxidant mechanism of TPs. TPs, tea polyphenols; ROS, reactive oxygen species; Nrf2, nuclear factor (erythroid-derived 2)-like 2; Mst, mammalian STE20-like protein kinase; HO-1, heme oxygenase 1; Keap1, Kelch-like ECH-associated protein 1; ARE, antioxidant response element; SOD, superoxide dismutase; GSH-Px, glutathione peroxidase; CAT, catalase; NO, nitric oxide; MDA, malondialdehyde; Maf, musculoaponeurotic fibrosarcoma; ARE, antioxidant response element.