Figure 6.

CHE inhibits the activation of p38 MAPK during H₂O₂-induced oxidative stress, and p38 MAPK inhibition mediates CHE-induced Nrf2 activation. (A) ARPE-19 cells were treated with or without 5 μM CHE for 2 h and then treated with H₂O₂ for 30 min. (C) Cells were pre-treated with a specific kinase inhibitor (PD98059 (ERK), SP600125 (JNK), SB203580 (p38), or LY 294002 (PI3K)) at 10 μM for 2 h, 5 μM CHE for another 2 h, and then followed by treatment with 500 μM H₂O₂ for 24 h. Cell viability was quantified via the CCK-8 assay. (D) ARPE-19 cells were pre-treated with a p38 inhibitor at 10 μM for 2 h, 5 μM CHE for another 2 h, and then treated with 500 μM H₂O₂ for 24 h. The protein levels of p38, pp38, HO-1, NQO-1, and Nrf2 were assessed via Western blotting. (B,E) The quantitative analysis of the p38, pp38, HO-1, NQO-1, and Nrf2 levels was performed via densitometric measurements relative to the control. ** p < 0.01, *** p < 0.001, versus control group; ## p < 0.01, ### p < 0.001, versus the H₂O₂-treated group; ++ p < 0.01, +++ p < 0.001, versus the H₂O₂ and chrysoeriol-treated group.