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. 2012 Aug 1;18(1):53–63. doi: 10.1007/s12192-012-0356-0

Fig. 3.

Fig. 3

a GM-CSF mRNA levels rise in rHSP27-treated macrophages. PMA-differentiated THP-1 cells were treated with media (control), rC1 (9.6 μM), or rHSP27 (9.6 μM) ± BAY 11-7082 (10 μM) for 24 h. Inhibition of NF-κB signaling was achieved by pre-treating the cells for 1 h with BAY 11-7082 (10 μM). All treatments were supplemented with Polymyxin B (PMB, 10 μg/mL). One-way ANOVA *p < 0.001); n = 3. b GM-CSF is secreted by THP-1 macrophages in response to rHSP27. PMA-differentiated THP-1 cells were treated with media, LPS (10 ng/mL), rHSP27 (9.6 μM), or rC1 (9.6 μM) ± BAY 11-7082 (10 μM) for 24 h. Inhibition of NF-κB signaling was achieved by pre-treating the cells for 1 h with BAY 11-7082 (10 μM). Polymyxin B (PMB, 10 μg/mL) was used as indicated. One-way ANOVA *p < 0.001; n = 3. c IL-10 is secreted by THP-1 macrophages in response to rHSP27. THP-1 macrophages were treated with media, LPS (10 ng/mL), rHSP27 (9.6 μM), or rC1 (9.6 μM) ± BAY 11-7082 (10 μM) for 24 h. Inhibition of NF-κB signaling was achieved by pre-treating the cells for 1 h with BAY 11-7082 (10 μM). Polymyxin B (PMB, 10 μg/mL) was used as indicated. One-way ANOVA *p < 0.001; n = 3