Fig. 2.

Telmisartan mediates its inhibitory effects on the tumor necrosis factor alpha (TNF-α)-induced expression of intercellular adhesion molecule-1 (ICAM-1) by the peroxisome proliferator-activated receptor gamma (PPARγ)-independent pathway. (A) GW9662 does not block the telmisartan-mediated effect. U87MG cells were either untreated, pre-treated with the PPARγ antagonist GW9662 (5 µM) or telmisartan (40 µM), or co-treated with telmisartan and GW9662 for 1 h and then further treated with 10 ng/mL TNF-α for 24 h. Whole cell lysates were analyzed by Western blotting. The error bars represent mean ± SEM (n=4). Statistical differences were determined using the student’s t-test. **p<0.01, ***p<0.001. (B) GW9662 does not alter TNF-α-induced ICAM1expression. U87MG cells were treated as describe in (A).