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 NFkappaB activation. The activation of NFkappaB by acrolein was induced as a result of degradation of IkappaBalpha 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.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Sarkar P,Hayes BEdoi
10.1007/s11010-007-9411-zsubject
Has Abstractpub_date
2007-07-01 00:00:00pages
191-9issue
1-2eissn
0300-8177issn
1573-4919journal_volume
301pub_type
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