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. 2017 Feb 1;174(22):4055–4069. doi: 10.1111/bph.13685

Figure 5.

Figure 5

Effect of AVE0991 on TNF‐α activated THP‐1 cytokine and chemokine mRNA expression, chemotaxis towards human adipocytes and chemokine expression in human adipocytes. (A) Expression of selected pro‐inflammatory mRNA cytokines and chemokines in THP‐1 cells stimulated with TNF‐α (10 ng·mL‐1) in presence of AVE0991 (1 μM) and/or the Mas receptor antagonist A779 (5 μM) (n = 6). (B) Chemotactic properties of THP‐1 cells stimulated with TNF‐α to supernatants from SW872 adipocyte cultures, stimulated with TNF‐α in absence or presence of AVE0991 (1 μM). Cell chemotaxis was analysed and expressed as a fold change of the number of cells passing through 8 μm pores under different conditions, compared with THP‐1 cells stimulated with TNF‐α (10 ng mL‐1) and with supernatants from native SW872 adipocytes without additional treatment. Before testing chemotaxis, the THP‐1 cells were stimulated for 6 h with TNF‐α or stimulated with TNF‐α for 6 h and then incubated with AVE0991 (1 μM) for 18 h (n = 5). (C) Expression of pro‐inflammatory CCL2, CCL5 and IL6 mRNA in SW872 cells differentiated to adipocytes and stimulated with TNF‐α (10 ng cm−3) or saline (CTRL), with or without AVE0991 (1 μM) (n = 6); * P < 0.05, significantly different as indicated; t‐ test.