Abstract
Chronic exposure to ultraviolet B (UVB) is a major cause of skin aging. The aim of the present study was to determine the photoprotective effect of a 30% ethanol extract of Eisenia bicyclis (Kjellman) Setchell (EEB) against UVB-induced skin aging. By treating human dermal fibroblasts (Hs68) with EEB after UVB irradiation, we found that EEB had a cytoprotective effect. EEB treatment significantly decreased UVB-induced matrix metalloproteinase-1 (MMP-1) production by suppressing the activation of mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) signaling and enhancing the protein expression of tissue inhibitors of metalloproteinases (TIMPs). EEB was also found to recover the UVB-induced degradation of pro-collagen by upregulating Smad signaling. Moreover, EEB increased the mRNA expression of filaggrin, involucrin, and loricrin in UVB-irradiated human epidermal keratinocytes (HaCaT). EEB decreased UVB-induced reactive oxygen species (ROS) generation by upregulating glutathione peroxidase 1 (GPx1) and heme oxygenase-1 (HO-1) expression via nuclear factor erythroid-2-related factor 2 (Nrf2) activation in Hs68 cells. In a UVB-induced HR-1 hairless mouse model, the oral administration of EEB mitigated photoaging lesions including wrinkle formation, skin thickness, and skin dryness by downregulating MMP-1 production and upregulating the expression of pro-collagen type I alpha 1 chain (pro-COL1A1). Collectively, our findings revealed that EEB prevents UVB-induced skin damage by regulating MMP-1 and pro-collagen type I production through MAPK/AP-1 and Smad pathways.
Highlights
The effects of sunlight on the skin are profound and are thought to account for up to 90% of visible skin aging [1]
Eisenia bicyclis (Kjellman) Setchell (EEB) recovered the ultraviolet B (UVB)-reduced expression of tissue inhibitors of metalloproteinases (TIMPs)-1 and TIMP-2 in a concentration-dependent manner (Figure 3D). These results indicate that EEB reduces UVB-induced matrix metalloproteinase-1 (MMP-1) expression by regulating the mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) signaling pathway and TIMP expression
The phosphorylation and total expression of Smad2/Smad3 were decreased by UVB irradiation, whereas EEB upregulated these reductions in a concentration-dependent manner. These results indicate that EEB recovers UVB-induced collagen degradation by activating the Smad signaling pathway
Summary
The effects of sunlight on the skin are profound and are thought to account for up to 90% of visible skin aging [1]. Periodic and continuous exposure to ultraviolet (UV) radiation is a classical and critical factor that contributes to skin aging, known as photoaging. Photoaging is characterized by wrinkles, inflammation, pigmentation, sagging, and dryness. UVB accounts for only a small portion of the total UV radiation, it is the most active at damaging the epidermis and dermis of the skin [2]. Several studies have reported that UVB irradiation increases intracellular reactive oxygen species (ROS), such as superoxide anions, hydroxyl free radicals, and hydrogen peroxide [3]. ROS stimulate various signaling pathways and initiate biological processes, including cell death, cellular senescence, and inflammation [4].
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