Figure 6.

(A) Intrinsic pathway of oxidative stress in HaCaT keratinocytes was induced with H₂O₂. Enhancement of H₂O₂ stimulated ROS production led to the protein’s expression of the p53, Bax, cytochrome C, caspase-9 and caspase-3 due to inhibition anti-apoptotic of Bcl-2. (B) The molecular mechanism of compound 1 inhibited H₂O₂-induced oxidative stress and increased antioxidant enzymes (GPx, and CAT) and level of non-enzymatic antioxidants activities (GPx) in HaCaT keratinocytes. The intracellular ROS production was decreased from compound 1, GPx, CAT, and GSH. These lead to the decrease of p53, Bax, cytochrome C, caspase-9 and caspase-3 levels and the increase of the anti-apoptotic of Bcl-2 protein.