Induction of COX-2 by acrolein in rat lung epithelial cells |
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Authors: | Poonam Sarkar Barbara E Hayes |
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Institution: | (1) College of Pharmacy and Health Sciences, Texas Southern University, 3100 Cleburne Street, Houston, TX 77004, USA |
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Abstract: | Acrolein is a highly reactive alpha, beta-unsaturated aldehyde, and a product of lipid peroxidation reactions. Acrolein is
also an environmental pollutant and a key component of cigarette smoke, and has been implicated in multiple respiratory diseases.
Lung tissue is a primary target for acrolein toxicity in smokers and may lead to chronic lung inflammation and lung cancer.
Chronic inflammation, associated with expression of cyclooxygenase-2 (COX-2) and prostaglandins, are predisposing factors
for malignancy. In this study, we investigated the induction of COX-2 by acrolein in rat lung epithelial cells and its related
signaling cascade. Induction of COX-2 by acrolein was significant at 6 h post-treatment and was dependent upon NFκB activation.
The activation of NFκB by acrolein was induced as a result of degradation of IκBα over the time of treatment. In addition,
the upstream signaling cascade involved Raf-1/ERK activation by acrolein in the COX-2 induction and was inhibited by GW5074
(a Ras/Raf-1/ERK inhibitor), thereby providing evidence for the role of this cascade in this process. The results of these
studies offer an explanation for the mechanism of COX-2 induction by acrolein in rat lung epithelial cells. |
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Keywords: | Acrolein COX-2 NF-κ B Cell proliferation |
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