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Bioorg Med Chem. 2011 Nov 1;19(21):6348-55. doi: 10.1016/j.bmc.2011.08.067. Epub 2011 Sep 5.

Sodium dl-α-tocopheryl-6-O-phosphate inhibits PGE₂ production in keratinocytes induced by UVB, IL-1β and peroxidants.

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Laboratory of Physiological Chemistry, Institute of Medicinal Chemistry, Hoshi University, Shinagawa, Tokyo 142-8501, Japan.


The water-soluble vitamin E derivative, sodium dl-α-tocopheryl-6-O-phosphate (1), exhibits protective effects against skin damage. As reported herein, we investigated the actions of 1 on the formation of the inflammatory mediator, prostaglandin E(2) (PGE(2)), as compared to dl-α-tocopheryl acetate (2) and dipotassium glycyrrhizin acid (3). In a three-dimensional (3D) human skin model 1 was converted to α-tocopherol (Toc) to a greater extent than 2. Post-treatment using 2% 1 following ultraviolet B (UVB) irradiation for 2h significantly reduced photodamage as indicated by UVB-damaged cell formation and PGE(2) synthesis. In normal human epidermal keratinocytes stimulated with UVB irradiation, or exposed to interleukin-1 beta, tert-butylhydroperoxide or hydrogen peroxide, pre-treatment with 1 (0-2 μM) inhibited PGE(2) production in dose-dependent manner to a greater extent than 2 and 3. Increases in stimulator-induced cyclooxygenase 2 mRNA expression and p38 MAPK phosphorylation were suppressed by pre-treatment with 1. The vitamin C derivative, magnesium L-ascorbyl-2-phosphate, significantly and synergistically, enhanced the inhibitory effects of 1 on PGE(2) production. These results suggest that 1 is a highly potent protective when compared among the examined commercial human skin care products, and that it might be useful for therapeutic and preventive medicine.

[Indexed for MEDLINE]

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