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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: J Pharmacol Sci. 2010 Mar 20;112(4):467–472. doi: 10.1254/jphs.09346sc

Fig. 3.

Fig. 3

Effects of various pharmacological inhibitors on the IL-13– induced increase in promoter activity of the rat RhoA gene. Cultured human bronchial smooth muscle cells were transfected with a luciferase reporter plasmid D3 (see Fig. 2), and luciferase assays were performed with (closed column) or without (open column) stimulation with 100 ng/mL of IL-13 in the presence or absence of various pharmacological inhibitors. AS: AS1517499 (100 nM, a selective STAT6 inhibitor), JAKs-I: JAK Inhibitor-I (1 μM, a non-selective JAKs inhibitor), AG490: tyrphostin-AG490 (50 μM, a selective JAK2 inhibitor), AG9: tyrphostin-AG9 (50 μM, a selective Tyk2 inhibitor), WHI: WHI-P131 (100 μM, a selective JAK3 inhibitor), and DMSO: dimethyl sulfoxide (0.1%, vehicle for the inhibitors). Each column represents the mean ± S.E.M. from 5 independent experiments. *P < 0.05 vs. no IL-13 treatment (open column), #P < 0.05 and ##P < 0.01 vs. DMSO–IL-13 group (closed column) by Bonferroni/Dunn’s test.