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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. 2.

Fig. 2

Telmisartan (Telm) inhibited lipopolysaccharide (LPS)-induced pro-inflammatory responses in human monocytes. Human monocytes were pre-incubated for 2 h with vehicle (DMSO) or Telm and subsequently exposed to 50 ng/ml LPS. (a) Expression of pro-inflammatory marker mRNA 2 h after LPS addition. (b) Cyclooxygenase-2 (COX-2) protein expression and cumulative prostaglandin E2 (PGE2) release in monocytes exposed to LPS for 24 h as determined by western blot and EIA, respectively. COX-2 protein expression was determined by western blot and quantified by densitometry. Values are presented as percentage of DMSO-treated group, as means ± SEM from at least three independent experiments. ***P<0.001 vs. DMSO; #P<0.05 vs. LPS. Picture shows a representative western blot. (c) Reactive oxygen species (ROS) production was determined by dichlorodihydrofluorescein diacetate probe oxidation in monocytes pretreated with vehicle or 10 μmol/l Telm and then exposed to LPS for 2 h. (d) Cell migration assay was performed on THP-1 monocytic cells pretreated with vehicle or 10 μmol/l Telm and subsequently stimulated with 100 ng/ml monocyte chemotactic protein-1 (MCP-1) for 4 h. Results are means ± SEM from at least three independent experiments. **P<0.01 vs. DMSO; ***P<0.001 vs. DMSO; #P<0.05 vs. LPS; ##P<0.01 vs. LPS; ###P<0.001 vs. LPS or MCP-1. ICAM-1, intercellular adhesion molecule 1; LOX-1, lectin-like oxidized low-density lipoprotein receptor-1.