Fig 2: Effects of TPs on the Mst-Nrf2 axis and Keap1/Nrf2/HO-1 pathway protein expression on RAW264.7 cells under oxidative damage. (A) The protein expression levels were tested using western blotting. (B) Keap1, (C) Mst2, (D) Mst1, (E) Nrf2 and (F) HO-1 proteins levels were quantified via densitometry and were normalized to β-actin. Each bar represents the mean ± SD of three independent experiments. *P<0.05 or **P<0.01 vs. the control group, ##P<0.01 vs. the H2O2 group. TPs, tea polyphenols; Mst, mammalian STE20-like protein kinase; Nrf2, nuclear factor (erythroid-derived 2)-like 2; Keap1, Kelch-like ECH-associated protein 1; HO-1, heme oxygenase 1.

Fig 3: 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.