TM reduces the CHIKV-induced inflammatory response through the MAPK pathway, NF-κB, and COX-2. RAW 264.7 cells were infected with CHIKV-IS, treated with TM (50 μM), GW (20 μM), and AG (20 μM) then harvested at 8 h pi. (A) Western blot showing the nsP2, PPAR-γ, and AT1 proteins levels along with phosphorylation status of p38, ERK, JNK, cJUN, IRF3, and NF-κB in RAW 264.7 cell lysates. Actin was used as a loading control. (B to I) Bar diagrams indicating relative band intensities of p-p38, p-ERK, p-JNK, p-cJUN, p-IRF3 p-NF-κB, PPAR-γ, and AT1 (J) Western blot showing the level of COX-2 protein. (K) Bar diagrams depicting relative band intensities of COX-2 protein. (L and M) Bar diagram showing the levels of secreted cytokines (TNF-α and IL-6) of CHIKV-infected and TM-treated macrophages in the supernatants quantified using sandwich ELISA of CHIKV-infected and TM-treated macrophages. Data represented mean ± SE (n = 3; P ≤ 0.05 was considered statistically significant).