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. 2007 Jun 18;51(9):3367–3370. doi: 10.1128/AAC.00041-07

FIG. 3.

FIG. 3.

RA abrogates the increased expression of proinflammatory mediators. (A) Expression of IL-12, TNF-α, IFN-γ, MCP-1, and IL-6 was observed by CBA in control animals, JEV-infected animals, JEV-infected and RA-treated animals, animals treated with RA alone, and JEV-infected and RA-treated animals at death. Levels of IL-12, TNF-α, IFN-γ, MCP-1, and IL-6 were significantly reduced in RA-treated samples compared to levels in infected mice. P < 0.001 (mean ± SEM). JEV-infected mice that succumbed even after RA treatment had significantly high levels of proinflammatory cytokines compared to uninfected mice. P < 0.001 (mean ± SEM) (four mice for each group). (B) Protein levels of control, JEV-infected, JEV-infected and RA-treated, RA-treated, and JEV-infected and RA-treated animals at death were analyzed by immunoblotting. Significant reductions in the levels of pNF-κB and Cox-2 in RA-treated samples were observed compared to levels in infected samples (P < 0.05). RA treatment reversed the level of IκB-α (P < 0.05). Mice that died even after RA treatment had increased levels of pNF-κB and Cox-2 and decreased levels of IκB-α compared to the control group. Data shown are for two individual animals from a total of four animals in each group.