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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: J Hypertens. 2012 Jan;30(1):87–96. doi: 10.1097/HJH.0b013e32834dde5f

Fig. 5.

Fig. 5

Peroxisome proliferator-activated receptor-γ (PPARγ) gene silencing eliminated the effect of telmisartan (Telm) on lipopolysaccharide (LPS)-induced gene expression in THP-1 cells. Human PPARγ-specific or nontargeting scrambled control small interfering RNA (siRNA) were transfected into THP-1 cells. PPARγ protein levels were measured at 48 and 72 h posttransfection by western blot (a). PPARγ mRNA expression (b) and cluster of differentiation 36 (CD36) and ATP-binding cassette subfamily G member 1 (ABCG1) mRNA expression (c) were measured at 72 h of posttransfection by real-time PCR. ***P<0.001 vs. scrambled siRNA or DMSO; ###P<0.001 vs. Telm. The inflammatory markers tumor necrosis factor-α (TNFα) and inhibitor of κB-α (IκB-α) were measured in cells treated for 2 h with LPS (50 ng/ml) alone or in a combination with 10 μmol/l Telm with and without PPARγ siRNA transfection (d). Results are means ± SEM from three independent experiments. ###P<0.001 vs. LPS; ***P<0.001 vs. LPS with Telm.