1106 Inhibition of cellular senescence by apocynin in human keratinocytes irradiated with ultraviolet b

Backgrounds: Ultraviolet radiation (UV) causes the process of cellular senescence mediated by oxidative stress and DNA damage, resulting in skin photoaging. Apocynin, an NADPH oxidase inhibitor can chemically induce Type 17 collagen (COL17) protein synthesis, which is crucial preventing aging. Our unpublished data showed that klotho mutant mice, a premature aging model, displayed increased senescence-associated-β-galactosidase (Sa- -Gal) activity, p16, phosphorylated histone H2AX (γH2AX), matrix metallopeptidase 9 1 (MMP-9, MMP-1), activation p38 mitogen-activated kinase (p38 MAPK) along with deceased COL17 production skin. objective was to investigate whether induction apocynin decrease UVB-induced cell senescence. Methods: The hTert-immortalized keratinocytes (KER-CT) were exposed UVB (100 J/m2) after being pretreated (10μM, 20 μM, 40 μM) for 24 hours. Immunohistochemistry, immunofluorescence, qRT-PCR, western blot used measure expression COL17, p38MAPK, MMP-9, MMP-1, p53, p21, γH2AX. Cellular measured SA-β-gal staining. Propidium iodide ((PI)/RNase solution cycle. Results: exposure decreased (P<0.05), phosphorylation Sa-β-Gal activity (P<0.001), G1 arrest p21 γH2AX (P<0.001) compared control group. Apocynin restored reduced cycle suppressed H2AX, p53 induced human (P<0.001). Conclusions: senescence, vitro restoring inhibiting oxidase.