Telmisartan is an angiotensin-II type 1 receptor (AT1R) blocker, currently used to treat patients with hypertension. Telmisartan, in addition to its effect on AT1R, is thought to activate the nuclear transcription factor, peroxisome proliferator-activated receptor-c (PPAR c), thereby acting as a partial PPARc agonist. This study was conducted to examine whether telmisartan might suppress cytokine-induced inflammatory signaling in vascular endothelial cells, thereby attenuating cellular inflammation possibly by PPARc activation. Telmisartan caused a dose-dependent suppression of the tumor necrosis factor-a (TNFa)-induced activation of nuclear factor (NF)-jB in vascular endothelial cells in this study. The PPARc antagonist, GW9662, did not influence the inhibitory effect of telmisartan on NF-jB activation. The thiazolidinediones neither influenced TNFa-induced NF-jB activation nor influenced the inhibitory effect of telmisartan in this process. Telmisartan dose dependently diminished the TNFa-induced gene expression of VCAM-1, and GW9662 did not attenuate this effect. Thus, telmisartan inhibits the cytokine-induced expression of the VCAM-1 gene by blocking NF-jB activation independently of PPARc activation. Although the mechanism by which this occurs remains unclear, our findings suggest that telmisartan-induced anti-inflammatory effects might have favorable effects on vasculature in hypertensive patients.
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