PubMed日本語 - EM、EM703ヒトの気管支上皮細胞でディーゼル排気粒子から酸化ストレスによって誘発されるNF-kB活性化を阻害する:IL-8転写の重要性。―QLifePro医療翻訳医療翻訳 QLifePro


EM, EM703 inhibit NF-kB activation induced by oxidative stress from diesel exhaust particle in human bronchial epithelial cells: Importance in IL-8 transcription.


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Ying-Ji Li, Takako Shimizu, Yukiyo Hirata, Hirofumi Inagaki, Hajime Takizawa, Arata Azuma, Tomoyuki Kawada, Isamu Sugawara, Shoji Kudoh, Toshiaki Sunazuka, Satoshi Omura


Department of Hygiene and Public Health, Nippon Medical School, Tokyo 113-8602, Japan. Electronic address:


Diesel exhaust particle (DEP) is the major components of PM2.5, and much attention has focused on PM2.5 in relation to adverse health effects, and many pulmonary diseases. In the present study, we used a human bronchial epithelial cell line (HBEC) to investigate the anti-inflammatory effects of erythromycin (EM) and EM703 - a new derivative of erythromycin without antibacterial effects on the expressions of IL-8 caused by DEP exposure. DEP showed a dose-dependent stimulatory effect on IL-8 product in BET-1 cell. Increases of IL-8 expression by DEP stimulation were significantly blocked by both EM and EM703 pretreatment. Furthermore, NF-κB and Nrf2 activation, the antioxidant enzymes such as HO-1, NQO-1 mRNA expression were increased by DEP exposure and these increases were blocked by both of EM and EM703 pretreatment. Our results suggest that, EM and EM703 may have an inhibitory effect on expression inflammatory cytokines in HBEC induced by DEP not only as an anti-inflammation but also an antioxidant drug. EM and EM703 might contribute to chemical prevention of the risk of pulmonary diseases induced by oxidative stress from environmental pollutant, such as DEP.


本研究において、我々は、エリスロマイシン(EM)とEM703 ― DEP暴露に起因するIL-8の発現に対する抗菌効果のないエリスロマイシンの新しい派生物 ― の抗炎症効果を調査するために、ヒトの気管支上皮細胞系(HBEC)を使用した。
さらにまた、NF-κBとNrf2活性化(HO-1のような抗酸化体酵素)である、NQO-1 mRNA発現はDEP暴露によって増加した、そして、これらの増加はEMとEM703前処置の両方ともによって妨げられた。

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