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Cyclooxygenase (COX)-2 and its products, including PGE2, are key inflammatorymediators. In this study, we have assessed the pharmacological characteristicsof BAI, a 3-aminoindazole derivative and a novel cyclin-dependent kinase (CDK)inhibitor, for regulation of COX-2 expression induced by interleukin (IL)-1β inA549 human airway cells. Treatment with BAI strongly inhibited IL-1β-induced expressionof COX-2 at both the protein and mRNA levels. Results of luciferase experimentsalso revealed that BAI treatment reduced IL-1β-induced COX-2 promoter activity.Distinctly, treatment with BAI did not affect IL-1β-induced phospho-rylation ofextracellular signal-regulated protein kinase-1/2 (ERK-1/2), p38 mitogen-activatedprotein kinase (MAPK), and c-Jun N-terminal protein kinase-1/2 (JNK-1/2) and proteolysisof IκB-α, an inhibitor of nuclear factor (NF)-κB, but inhibited IL-1β-inducedphosphorylation of histone H1, a target for phosphorylation by CDKs. siRNA transfectionexperiments demonstrated that knockdown of CDK2 and CDK4 led to a slight reductionof IL-1β-induced histone H1 phosphorylation but had no effect on IL-1β-inducedCOX-2 expression. Interestingly, additional cell culture experiments showed theability of BAI to repress the PMA-induced COX-2 expression in A549 cells and serum-dependentCOX-2 expression in NCI-H292 cells, a human laryngeal cell line. Collectively,these results demonstrate firstly that BAI downregulates IL-1β-induced COX-2 expressionthrough transcriptional repression, which appears to be independent of CDK2, CDK4,MAPKs and NF-κB, in A549 cells. It is suggested that BAI may be a potential candidatefor treatment of the airway inflammatory diseases where COX-2 overexpression isproblematic.

BAI, a 3-aminoindazole derivative, inhibits interleukin-1β-induced expression of cyclooxygenase-2 in A549 human airway cells