520 The protective effects of Apocynin against ultraviolet B-induced cellular senescence in human keratinocytes

Cellular senescence is an irreversible growth arrest caused by oxidative stress and DNA damage ultraviolet (UV) radiation mediated cellular responsible for skin photoaging. Type 17 collagen (COL17) crucial preventing aging. Apocynin, a NADPH oxidase inhibitor can chemically induce COL17 protein synthesis promote stem cell survival. Our unpublished data showed that klotho mutant (kl/kl) mice, which premature aging model, displayed increased senescence-associated-β-galactosidase (Sa-β-Gal) activity, production of p16, phosphorylated histone H2AX (γH2AX), matrix metallopeptidase 9 1 (MMP-9, MMP-1), activation mitogen-activated kinase (MAPK) along with deceased in the skin. study aimed to investigate whether induction apocynin decrease UVB-induced or not. In our experimental model hTert/KER-CT keratinocytes were pretreated (10 μM, 20 40 μM) 24 hours exposed UVB (100 J/m2). Immunohistochemistry, immunofluorescence, qRT-PCR, western blot used measure expression COL17, MAPK, MMP-9, MMP-1, γH2AX, was measured SA-β-gal staining, propidium iodide ((PI)/RNase solution cycle. study, exposure decreased (P<0.05), Sa-β-Gal activity (P<0.001), G1 p16 γH2AX (P<0.001). Apocynin restored (P<0.01) reduced cycle (P<0.01), suppressed human The change at level parallel mRNA expression. Taken together, results suggest damage, senescence, it also thereby protected cells from