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K. Ohgami, K. Shiratori, I.B. Ilieva, K. Yazawa, S. Ohno; The effects of astaxanthin on lipopolysaccharide–induced inflammation in vitro and in vivo . Invest. Ophthalmol. Vis. Sci. 2004;45(13):573.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:Several previous studies have demonstrated that Astaxanthin (AST), a carotenoid that is found in marine organisms, exhibits a wide variety of biological activities including antioxidant and anti–tumor effects. We previously reported that AST shows dose–dependent anti–ocular inflammatory effects in vivo. In order to elucidate the anti–inflammatory mechanism of AST, the present study was to investigate the efficacy of AST on the levels of prostaglandin E2 (PGE2), nitric oxide (NO), tumor necrosis factor–α (TNF–α) and expression of cyclooxygenase–2 (COX–2) protein, inducible nitric oxide synthase (iNOS) protein in the mouse macrophage cell line (RAW264.7).Methods:RAW 264.7 cells with various concentrations of AST were incubated with 10 µg/ml of lipopolysaccharide (LPS) for 24 hours. Levels of PGE2 and TNF–α as well as NO production in medium were determined. COX2 and iNOS protein expression were analyzed by Western blotting method.Results: Concentrations of PGE2, TNF–α as well as levels of NO production in the AST group tended to decrease in a dose–dependent fashion. The expression of iNOS protein was suppressed to a similar degree by 25 µM of AST. Expression of COX–2 protein in the AST group tended to decrease in a dose–dependent fashion.Conclusion: The results of the present study suggest that AST reduces the levels of LPS–induced PGE2, TNF–α and NO in a dose–dependent manner. A possible mechanism of anti–inflammation effect of AST suppress not only NO production by blocking expression of NOS, but also PGE2 production by blocking expression of COX–2.
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