N-benzyl-N-methyldecane-1-amine derived from garlic ameliorates UVB-induced photoaging in HaCaT cells and SKH-1 hairless mice.

Skin tissue is susceptible to oxidative stress-induced senescence provoked by ultraviolet (UV) exposure in our daily lives, resulting in photoaging. Herein, we explore whether N-benzyl-N-methyldecan-1-amine (BMDA) derived from garlic ameliorates UVB-induced photoaging. To address this issue, HaCaT keratinocytes were exposed to UVB irradiation under BMDA treatment. The presence of BMDA substantially reduced UVB-induced ROS levels in a dose-dependent manner. BMDA administration counteracted UVB-induced senescence in the β-galactosidase assay. Treatment with BMDA also rescued UVB-exposed cells (S phase; from 18.3 to 25.8%) from cell cycle arrest, similar to the level observed in untreated normal cells. These findings might support our observation that elevated levels of γ-H2AX, a DNA damage marker, under UVB exposure were reduced following BMDA administration. Additionally, BMDA treatment indirectly reduced UVB-induced melanin synthesis in melanocytes since BMDA failed to inhibit tyrosinase activity, a crucial enzyme in melanin synthesis. The topical application of BMDA on the skin of SKH-1 hairless mice also diminished wrinkle formation, supported by recovered collagen levels and the thickness of the epidermis and dermis, compared to those of UVB-control mice. Finally, the BMDA treatment diminished the expression of inflammatory cytokine transcripts such as TNF-α, IL-1β, IL-4, and IL-6 in the UVB-exposed skin tissues. This finding is further supported by Immunofluorescence microscopy, which showed a decrease in the expression of TNF-α, and IL-1β during BMDA treatment. Altogether, as BMDA mitigates UVB-induced photoaging by reducing ROS production, protecting against DNA damage, and suppressing inflammatory cytokine production, it has been proposed as an effective anti-photoaging molecule.