Fig. 5

Effects of dexamethasone (DEX) on CXCL8 production in acidic pH or TNF-α-stimulated ASMCs. a ASMCs were pretreated with DEX (10^− 12-10^− 6 M) or control vehicle (0.1% ethanol) for 30 min. The cells were further incubated at the indicated pH with DEX or control vehicle for 24 h. DEX inhibits CXCL8 production of acidic pH-stimulated ASMCs in a dose-dependent manner. Its inhibition is significant at 1 nM and over of DEX. Data are expressed as percentages of CXCL8 values in the supernatants of pH 6.3-stimulated ASMCs without DEX (mean ± SEM, n = 4; **, P < 0.01). b DEX (1 μM) significantly inhibits CXCL8 mRNA expression in ASMCs at 5 h after acidic pH-stimulation. The expression levels of CXCL8 mRNA are standardized to those of GAPDH mRNA. Data are expressed as percentages of CXCL8 mRNA expression at 5 h after pH 6.3-stimulation (mean ± SEM, n = 3; **, P < 0.01). c TNF-α (1–100 ng/mL) induces CXCL8 secretion for 24 h in a dose-dependent manner. DEX (1 μM) partially but significantly inhibits CXCL8 production of TNF-α-stimulated ASMCs in each concentration of TNF-α. The inhibition rate of CXCL8 secretion by DEX in TNF-α-stimulated ASMCs seems to be smaller than that in acidic pH-stimulated ASMCs. Data are expressed as percentages of CXCL8 values of pH 6.3-stimulated ASMCs without DEX (mean ± SEM, n = 4; **, p < 0.01; *, P < 0.05; NS, not significant)