Abstract：
:Neutrophil accumulation response to cigarette smoke (CS) in humans and animal models is believed to play an important role in pathogenesis of many tobacco-related lung diseases. Here we evaluated the lung anti-inflammatory effect of aspirin and indomethacin in mice exposed to CS. C57BL/6 mice were exposed to four cigarettes per day during 4 days and were treated i.p. with aspirin or indomethacin, administered each day 1h before CS exposure. Twenty four hours after the last exposure, cells and inflammatory mediators were assessed in bronchoalveolar lavage (BAL) fluid and the lungs used for evaluation of lipid peroxidation, p38 mitogen-activated protein kinase (MAPK) phosphorylation and nuclear transcription factor kappaB (NF-kappaB) activation. Exposure to CS resulted in a marked lung neutrophilia. Moreover, the levels of oxidative stress-related lipid peroxidation, prostaglandin E(2) (PGE(2)), interleukin 1beta (IL-1beta), monocyte chemotactic protein 1 (MCP-1), and activated NF-kappaB and p38 MAPK were greatly increased in CS group. Aspirin or indomethacin treatment led to a significant reduction of neutrophil influx, but only aspirin resulted in dramatic decrease of inflammatory mediators. Moreover, both drugs reduced lung p38 MAPK and NF-kappaB activation induced by CS. These results demonstrate that short-term CS exposure has profound airway inflammatory effects counteracted by the anti-inflammatory agents aspirin and indomethacin, probably through COX-dependent and -independent mechanisms.
journal_name
Biochem Pharmacoljournal_title
Biochemical pharmacologyauthors
Castro P,Nasser H,Abrahão A,Dos Reis LC,Riça I,Valença SS,Rezende DC,Quintas LE,Cavalcante MC,Porto LC,Koatz VLdoi
10.1016/j.bcp.2008.12.012subject
Has Abstractpub_date
2009-03-15 00:00:00pages
1029-39issue
6eissn
0006-2952issn
1873-2968pii
S0006-2952(08)00892-7journal_volume
77pub_type
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