Suppressive effects of astaxanthin against rat endotoxin-induced uveitis by inhibiting the NF-kB signaling pathway

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  • Suppressive effects of astaxanthin against rat endotoxin-induced uveitis by inhibiting the NF-κB signaling pathway
  • Suppressive effects of astaxanthin against rat endotoxin-induced uveitis by inhibiting the NF-kappa B signaling pathway

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We investigated the effects of astxanthin (AST), a carotenoid, on endotoxin-induced uveitis (EIU), and measured the expression of inflammatory cytokines and chemokines in the presence or absence of AST over the course of the disease. EIU was induced in male Lewis rats by footpad injection of lipopolysaccharide (LPS). Immediately after the LPS inoculation, either 1, 10, or 100 mg/kg of AST were injected intravenously. Aqueous humor was collected at 6, 12 and 24 hours after LPS inoculation and the number of infiltrating cells in the anterior chamber were counted. In addition, we assayed the concentration of protein, nitric oxide (NO), tumor necrosis factor (TNF)- and prostaglandin (PG) E2. Immunohistochemical staining with a monoclonal antibody against activated NF-B was performed in order to evaluate the effects of AST on NF-B activation. Rats injected with AST showed a significant decrease in the number of infiltrating cells in anterior chamber. Moreover, AST-treated rats with EIU showed significantly lower concentrations of protein, NO, TNF- and PGE2 in the aqueous humor. Even the early stages of EIU were suppressed by injection of AST. The number of activated NF-B-positive cells was lower in iris-ciliary bodies treated with 10 or 100 mg/kg AST at 3 hours after LPS injection. These results suggest that AST reduces ocular inflammation in eyes with EIU by downregulating proinflammatory factors and by inhibiting the NF-B-dependent signaling pathway.

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