NIACINAMIDE DIMINISHED UVB INDUCED STRESS RESPONSE IN HUMAN EPIDERMAL EQUIVALENT MODEL.
Niacinamide (vitamin B3) is used in various skin care formulation, since it has been shown to photoprotective activities and effectiveness on sallowness, wrinkling, red blotchiness and hyperpigmented spots in aging skin. In order to investigate the molecular mechanism of this effect of niacinamide, we used EPI-201, a human skin equivalent model with partially formed stratified, cornified epidermis (purchased from MatTek). EPI-201 model was exposed to UVB with a single dose of 600 ml/cm2 and 2% niacinamide aqueous solution was added upper side of the model immediately after irradiation. Following 24 h of incubation, RNA and glutathione were extracted for measurement. UVB irradiation was induced gene expression of IL-1 alpha, heme oxygenase 1 (HO-1), Transglutaminase 1 (TGM1), and involcurin (IVL). Niacinamide suppressed the induction of IL-1 alpha and HO-1, while no significant effect on the induction of TGM1 and IVL was observed. UVB irradiation decreased intracellular glutathione level and niacinamide diminished this toxicity of UVB radiation. Nicotinic acid and niacinamide mononucleotide (NMN) did not show significant effect on UVB stress responses. And that is to say, the precursors of nicotinamide adenine dinucleotide (NAD) are not effective, except niacinamide. These data suggest that niacinamide may act on other pathways rather than on cellular energy repletion, although its molecular mechanism is unclear. It is noteworthy that niacinamide was effective when added after UVB irradiation. Niacinamide may act to suppress the prolonging of stress response and exert its photoprotective effect.
COSN, EPI-201, Glutathione, Herne oxygenase 1 (HO-1), IL-1a, Involcurin, Niacinamide (vitamin B3), Nicotinamide adenine dinucleotide, P13, PARP-1, Transglutaminase, UVB
Niacinamide mononucleotide, Nicotinic acid
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