Ultraviolet B (UVB) irradiation induces both production of reactive oxygen species (ROS) and glucocorticoids (GCs)-mediated stress responses such as an increase of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity in skin. In addition, ROS-induced inflammatory mediators and proinflammatory cytokines trigger skin inflammation. In this study, as 11β-HSD1 inhibitor recovered a decrease of catalase expression, we investigated whether Trapa japonica (TJ) extract and its fractions could inhibit 11β-HSD1/ROS-induced skin inflammation in HaCaT keratinocytes. TJ extract and its fractions inhibited expressions of 11β-HSD1 as well as the increase of ROS in UVB-exposed HaCaT keratinocytes. Moreover, proinflammatory cytokines such as interleukin (IL)-α, -β and tumor necrosis factor (TNF)-α, and cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) as inflammatory mediators were also inhibited in both mRNA and protein levels. Finally, prostaglandin E 2 (PGE 2 ) produced by COX-2 was inhibited effectively by TJ extract and its fractions. Taken together, these results suggest that TJ extract could be a potential anti-inflammatory ingredient to inhibit UVB-induced inflammation in skin.
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