목적: NF-kB, a dimeric transcription factor, is an important regulator of many immune and inflammatory process. Non-canonical pathway of NF-kB differs from canonical pathway in not only the composition of complex but also the signaling mechanism. This study assessed the role of NF-kB in the growth of the bacterially induced middle ear mucosa using inhibitors of the two NF-kB pathways. 방법:Otitis media was induced by inoculation of nontypeable Haemophilus influenza (NTHi) into the middle ear (ME) cavity of rats. Inflamed ME mucosal explants were cultured with caffeic acid phenethyl ester (CAPE), the inhibitor of NF-kB. Also, explants were treated with 1, 3(2H, 4H)-isoquinolinedione, the inhibitor of NF-kB inducing kinase. The area of explant outgrowth was measured daily and analyzed to 10 days in culture. 결과:The growth of NTHi induced ME mucosa was significantly inhibited by treating with CAPE in a dose-dependent manner. Also, ME mucosal explants treated with 1, 3(2H, 4H)-isoquinolinedione showed significantly suppressed growth responses in a dose-dependent manner compared with control explants. 결론:Inhibition of both canonical and non-canonical NF-kB pathway resulted in a diminished mucosal proliferative responses during bacterial OM in rats. These results support the role for NF-kB in the inflammatory and proliferative responses to NTHi infection of ME mucosal epitherium. Both canonical and non-canonical NF-kB signaling pathways are critical to the regulation of bacterially induced otitis media in rat.