FIG 10.

Schematic representation of proposed working model demonstrating the involvement of AT1, PPAR-γ, and MAPKs after TM treatment during CHIKV infection. Activation of AT1 and blocking of PPAR-γ induced higher phosphorylation of MAPKs with an increase in the expression of COX-2 and NF-κB that led to an increase in the level of inflammatory mediators (TNF-α and IL-6). Infection by CHIKV induced these axes to cause inflammation, tissue injury, and cell death. Both AG and GW increased CHIKV infection and inflammation. TM blocked AT1 and activated PPAR-γ to reduce CHIKV infection and inflammation.