Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8525298 | Biomedicine & Pharmacotherapy | 2018 | 9 Pages |
Abstract
Emphysema results in a proteinase - antiproteinase imbalance, inflammation and oxidative stress. Our objective was to investigate whether atorvastatin could repair mouse lungs after elastase-induced emphysema. Vehicle (50â¯Î¼L) or porcine pancreatic elastase (PPE) was administered on day 1, 3, 5 and 7 at 0.6â¯U intranasally. Male mice were divided into a control group (sham), PPE 32d (sacrificed 24â¯h after 32 days), PPE 64d (sacrificed 24â¯h after 64 days), and atorvastatin 1, 5 and 20â¯mg treated from day 33 until day 64 and sacrificed 24â¯h later (A1â¯mg, A5â¯mg and A20â¯mg, respectively). Treatment with atorvastatin was performed via inhalation for 10â¯min once a day. We observed that emphysema at day 32 was similar to emphysema at day 64. The mean airspace chord length (Lm) indicated a recovery of pulmonary morphology in groups A5â¯mg and A20â¯mg, as well as recovery of collagen and elastic fibers in comparison to the PPE group. Bronchoalveolar lavage fluid (BALF) leukocytes were reduced in all atorvastatin-treated groups. However, tissue macrophages were reduced only in the A20â¯mg group compared with the PPE group, while tissue neutrophils were reduced in the A5â¯mg and A20â¯mg groups. The redox balance was restored mainly in the A20â¯mg group compared with the PPE group. Finally, atorvastatin at doses of 5 and 20â¯mg reduced nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and matrix metalloproteinase-12 (MMP-12) compared with the PPE group. In conclusion, atorvastatin was able to induce lung tissue repair in emphysematous mice.
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Authors
Adriana Correa Melo, Isabella Cattani-Cavalieri, Marina Valente Barroso, Nicolas Quesnot, Lycia Brito Gitirana, Manuella Lanzetti, Samuel Santos Valença,