Suppression of γ-tocotrienol on UVB induced inflammation in HaCaT keratinocytes and HR-1 hairless mice via inflammatory mediators multiple signaling

Tocopherol (Toc) such as α-Toc has been expected to act as photochemopreventive agent of skin, but the effect of the other vitamin E forms [tocotrienols (T3)] has not been fully understood. We evaluated the anti-inflammatory effect of T3 on UVB-induced inflammatory reaction using immortalized human keratinocytes and hairless mice. γ-T3 suppressed UVB-induced PGE₂ production while similar ±-Toc doses had no effect. The anti-inflammatory actions of γ-T3 were explained by its ability to reduce UVB-induced inflammatory gene and protein expression [cyclooxgenase-2 (COX-2), interleukin (IL)-1β, IL-6, and monocyte chemotactic protein-1]. Western blot analysis revealed γ-T3 inhibited p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase/stress-activated protein kinase activation. In HR-1 hairless mice, oral T3 suppressed UVB-induced changes in skin thickness, COX-2 protein expression, and hyperplasia, but α-Toc did not. These results suggest T3 has potential use to protect against UVB-induced skin inflammation.