Telmisartan protects the Lipopolysaccharide Intoxicated Raw 264.7 Cell Line by Deactivating NFκB Mediated Inflammatory Mechanism

In addition to its AT1R (angiotensin receptor) blocking properties, telmisartan functions as a partial agonist at peroxisome proliferator-activated receptor-γ (PPARγ) which controls the expression of pro-inflammatory genes. We hypothesized that; in murine RAW 264.7 cell line, the anti-inflammatory effects of telmisartan may be mediated through PPARγ with NFκB deactivation. To test the hypothesis, the anti-inflammatory effect of telmisartan was assessed in lipopolysaccharide (LPS) intoxicated RAW 264.7 cells by MTT cytotoxicity assay. The protective effect was supported by the measuring transcription factor NFκB. The results indicate that telmisartan attenuated pro inflammatory mediator TNFα expression via NFκB deactivation and protected LPS intoxicated RAW 264.7 cell line. In conclusion the study indicates the existence of association between PPARγ and NFκB mediated inflammatory mechanism which was controlled by angiotensin receptor blocker telmisartan in RAW 264.7 cell line via NFκB deactivation effect.