Abstract
Long-term exposure to ultraviolet (UV) irradiation causes skin inflammation and aging. N-(4-bromophenethyl) caffeamide (K36H) possesses antioxidant and antimelanogenic properties. The present study investigated the effects of K36H on UVB-induced skin inflammation in human skin fibroblasts and hairless mice and evaluated the underlying mechanisms. The in vitro results indicated that K36H reduced UVB-induced mitogen-activated protein kinase (MAP kinase) expression. Furthermore, K36H treatment reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in UVB-irradiated fibroblasts by regulating IκB and nuclear factor-kappa B (NF-κB) expression. In the animal study, topically applied K36H markedly reduced inflammation and skin thickness and prevented photodamage to the skin of hairless mice. In addition, K36H inhibited the levels of UV-upregulated inflammation-related proteins levels such as IL-1, iNOS, and NF-κB in the dermis of hairless mice. Our findings demonstrated the antioxidant and anti-inflammatory properties of K36H in human skin fibroblasts and hairless mice. Therefore, K36H can be developed as an antiphotodamage and antiphotoinflammation agent.
Highlights
IntroductionSeveral studies have indicated that both ultraviolet (UV) A and UVB can cause skin photodamage by stimulating reactive oxygen species (ROS) generation, activating downstream signaling and inflammatory cytokine formation [2]
Exposure to sunlight can cause oxidative stress and inflammation, resulting in melanogenesis and mutations in skin cells; sun exposure can result in skin disorders and cancer [1].Several studies have indicated that both ultraviolet (UV) A and UVB can cause skin photodamage by stimulating reactive oxygen species (ROS) generation, activating downstream signaling and inflammatory cytokine formation [2]
Nuclear factor-κB (NF-κB) is translocated to the nucleus, where it regulates where it regulates inflammation-related gene transcription and protein expression, leading to inflammation-related gene transcription and protein expression, leading to inflammation and erythema inflammation and erythema of the skin [4,5]
Summary
Several studies have indicated that both ultraviolet (UV) A and UVB can cause skin photodamage by stimulating reactive oxygen species (ROS) generation, activating downstream signaling and inflammatory cytokine formation [2]. These cytokines subsequently activate mitogen-activated protein (MAP) kinase signaling and modulate downstream transcription factors, resulting in an inflammatory response [3]. Some proinflammatory factors and MAP kinases activate IκB kinase, Molecules 2017, 22, 1639; doi:10.3390/molecules22101639 www.mdpi.com/journal/molecules triggering IκB ubiquitination. UV irradiation leads to the generation of of the skin [4,5]. UV irradiation leads to the generation of ROS that attack biomembrane
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