Abstract:Objective: To investigate the effect of paeoniflorin (PF) on oxidative stress damage induced by hydrogen peroxide (H2O2) in skin fibroblasts (HSF) by regulating the silent information regulator 2 homologue 1 (SIRT1)/peroxisome proliferator activated receptor-gamma coactivator-1α (PGC-1α)/nuclear factor erythroid-derived 2-related factor 2 (Nrf2) signaling pathway.Methods: HSF cells were studied and separated into the Control group, H2O2 group, L-PF, M-PF, H-PF group, and PF+EX527 group. CCK-8 was applied to detect HSF cell proliferation. The β-galactosidase staining method was applied to detect HSF cell aging. Flow cytometry was used to detect apoptosis of HSF cells. ELISA method was used to detect the expression of ROS, SOD, GSH, and MDA in HSF cells. WB was used to detect the expressions of SIRT1, PGC-1α, and Nrf2 proteins in HSF cells.Results: The survival rate, SOD, GSH, SIRT1, PGC-1α, and Nrf2 expression of HSF cells in the H2O2 group were lower than in the control group, the proportion of aging cells, apoptosis rate, ROS, and MDA expression were higher than in the control group (P<0.05). Compared with the H2O2 group, the survival rate, SOD, GSH, SIRT1, PGC-1α, and Nrf2 expression were increased in the L-PF group, M-PF group, and H-PF group, the proportion of aging cells, apoptosis rate, ROS, and MDA expression were decreased (P<0.05). The survival rate, SOD, GSH, SIRT1, PGC-1α, and Nrf2 expression in the PF+EX527 group were lower than in the H-PF group, the proportion of aging cells, apoptosis rate, ROS, and MDA expression were higher than in the H-PF group (P<0.05).Conclusion: PF can inhibit H2O2-induced oxidative stress damage in HSF cells, and its mechanism may be achieved by activating the SIRT1/PGC-1α/Nrf2 signaling pathway.
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