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. Author manuscript; available in PMC: 2021 Apr 1.
Published in final edited form as: Antiviral Res. 2020 Feb 17;176:104749. doi: 10.1016/j.antiviral.2020.104749

Figure 6: Involvement of p38 activation on anisomycin antiviral activity.

Figure 6:

(A) Uninfected or (B) DENV-2 infected Vero cells were treated with different concentrations of anisomycin and p38 phosphorylation was analyzed by Western blot. The relative intensity of P-p38/p38 bands of each sample with respect to uninfected untreated cells is shown. GAPDH was revealed as loading control. U: uninfected cells, I: infected cells. (C and D) DENV-2 infected Vero cells untreated or treated with anisomycin (200 nM), SB202190 (16 μM) or a combination of both compounds were incubated for 24 h at 37°C. (C) p38 activation was analyzed by Western blot and the relative intensity of P-p38/p38 bands of each sample with respect to uninfected untreated cells is shown. GAPDH was used as loading control. (D) Viral yields were determined by plaque assay and results are expressed as percentage of inhibition in treated cells with respect to untreated infected cells. In (A), (B) (C) and (D) each value represents the mean ± SD of three independent experiments.