ANTI-INFLAMMATORY EFFECTS OF SALBUTAMOL ON HUMAN BRONCHIAL EPITHELIAL CELLS STIMULATED BY CIGARETTE SMOKE EXTRACT
DOI:
https://doi.org/10.18554/acbiobras.v6i1.7244Keywords:
Cigarette smoke extract, bronchial epithelial cells, smokingAbstract
Cigarette smoking, the major cause of chronic obstructive pulmonary disease (COPD), induces activation of pro-inflammatory pathways in the airway epithelium. Salbutamol, a selective and short-acting ?2-adrenoceptor agonist, is used for bronchospasm relief in patients with asthma and COPD. In addition, salbutamol also presents anti-inflammatory effects. Here, we evaluated whether salbutamol (10-5-10- 7 M) can reduce on bronchial epithelial cells (BEAS-2B cells) the inflammatory parameters induced by cigarette smoke extract (CSE; 1%). After 24h, Salbutamol reduced the IL-1? production induced by CSE in a concentration-response manner. Salbutamol (10-6 M) reduced the IL-8 production and increased the IL-10 production on CSE-stimulated cells. Also, salbutamol (10-6 M) decreased the ICAM-1 expression and the reactive oxygen species production. These anti-inflammatory effects could be associated with the down regulation of activation of NF-?B. Salbutamol may be a potential alternative treatment to airway inflammation caused by cigarette smoking such as in COPD patients.
Downloads
Published
Issue
Section
License
The author(s) retain(s) the rights to the published material. However, publication automatically implies the transfer of copyright, without payment from the journal. The author(s) transfer(s) their economic rights (the right to publish, reproduce, distribute) to the journal. The author(s) do not receive(s) financial remuneration from the Acta Biologica Brasiliensia journal for publishing; the consideration is the dissemination of their work. The author retains authorship (moral rights), but, to publish, transfers or licenses the rights of commercial/economic exploitation (economic rights) to the Acta Biologica Brasiliensia journal, free of charge, making the article open access or, in traditional models, the property of the publisher.
