Nobiletin enhances peroxiredoxin-1, preventing UVA radiation-induced oxidative stress and photoaging in human skin epidermal keratinocytes

Abstract

NBN is a bioflavonoid that counteracts the harmful effects of UVA radiation-induced cytotoxicity, reducing ROS production, DNA damage, and inhibiting apoptosis. NBN mitigates the signs of photoaging in HaCaT cells by downregulating the expression of MAPKs, AP-1, and MMPs while promoting collagen production. NBN enhances the Prdx-1 expression during the UVA-irradiation, thereby impeding the expression MAPKs, MMPs, AP-1, and downregulation of collagens, and Smad-3 in HaCaT cells. • UVA radiation induces MMPs and collagen degradation leads to photoaging. • NBN, a dietary flavonoid, enhances Prdx-I, thereby inhibiting antioxidant depletions. • NBN impedes UVA-mediated Photoaging responses by Prdx-I expressions. This study investigates the role of nobiletin (NBN), a dietary flavonoid preventing ultraviolet-A (UVA) radiation-induced oxidative damage and photoaging responses in skin epidermal keratinocytes (HaCaT). NBN treatment prevents cell toxicity, ROS, DNA damage, and apoptosis in UVA-exposed HaCaT cells. Furthermore, NBN prevents UVA radiation treatment-mediated overexpression of p-Erk-1, p-Jnk, p-p38, and AP-1 in HaCaT cells. Peroxiredoxin I (Prdx-1) is an antioxidant protein and enhanced activities of Prdx-1 have been considered a major target for inhibition of UVA radiation-mediated oxidative damage and photoaging responses. In this study, we noticed that NBN enhanced Prdx-1 expression, thereby enhancing antioxidants and inhibiting matrix metalloproteinase (MMP-1, MMP-2, MMP-9) and collagen degradation (Col-I and Col-III) in UVA-exposed HaCaT cells. Moreover, NBN treatment prevents UVA irradiation-induced downregulations of p-Smad and TGF-β1 expressions in HaCaT cells. In conclusion, our present results stated that NBN effectively prevents UVA-induced skin oxidative damage and photoaging responses through enhanced Prdx-1 expression.

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