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- W2070145105 abstract "Recent studies have shown that diesel exhaust particles (DEP) have adverse effects on the respiratory tract in vitro and in vivo, related to various pro-inflammatory cytokines and inflammatory mediators. The inflammation induced by the production of cyclooxygenase (COX)-2, an important mediator of inflammation and tumor promotion, and excess eicosanoids may be central to the pathogenesis of DEP-induced airway inflammation. However, the role of COX-2 in the pathogenesis of DEP-induced lung inflammation remains unclear, especially in vivo. In this study, we demonstrated that treatment with 50 μg/ml of DEP for 24 h induced the expression of the COX-2 gene at both the transcriptional and protein levels, which led to an increase in the release of prostaglandin E2 (PGE2) in A549 cells. In addition, the increased levels of COX-2 and PGE2 by DEP exposure were significantly suppressed by treatment with 50 pg/ml of dexamethasone (Dex). We also showed that exposure to 25 mg/kg of DEP induced the expression of the COX-2 protein in mouse lung tissues, and this increased COX-2 expression was attenuated by pretreatment with 5 mg/kg of Dex. These findings suggest that COX-2 may play an important role in the pathogenesis of DEP-induced pulmonary inflammation, which is effectively inhibited by glucocorticoid treatment." @default.
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- W2070145105 date "2008-02-15" @default.
- W2070145105 modified "2023-10-15" @default.
- W2070145105 title "COX-2 expression and inflammatory effects by diesel exhaust particles in vitro and in vivo" @default.
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- W2070145105 doi "https://doi.org/10.1016/j.toxlet.2007.11.005" @default.
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