RT Journal Article
SR Electronic
T1 Involvement of oxidative and nitrosative stress in the development of proteolytic pulmonary emphysema
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P3739
VO 40
IS Suppl 56
A1 Lanzetti, Manuella
A1 Costa, Cristiane
A1 Victoni, Tatiana
A1 Nesi, Renata
A1 Lopes, Alan
A1 Alves, Jackson
A1 Martins, Vanessa
A1 Resende, Angela
A1 Lagente, Vincent
A1 Porto, Luís
A1 Valenca, Samuel
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/P3739.abstract
AB Our aim was to investigate the participation of oxidative stress in elastase-induced pulmonary emphysema. C57BL/6 mice were submitted to pancreatic porcine elastase (PPE) instillation (0.05U or 0.5U) per mouse (i.t.) to induce pulmonary emphysema. A separated group of mice were treated with aminoguanidine 1% (AMG). Lungs were collected on days 7, 14 and 21 after PPE instillation. Control group was sham-injected. We performed BAL, biochemical analyses of oxidative stress, and lung stereology and morphometry. Emphysema was histologically characterized at 21 days after 0.5 U of PPE, presenting increased alveolar linear intercept and volume density of airspaces in comparison with the control group. TNF-α was elevated at 7 and 14 days after PPE 0.5 U, concomitant with reduction in the IL-10 levels at the same time-points. Myeloperoxidase was elevated in all groups treated with 0.5 U of PPE. A contribution of oxidative stress at early stage of emphysema was observed with increased levels of nitrite, malondialdehyde and superoxide dismutase activity at 7 days after PPE 0.5 U. Glutathione peroxidase activity was increased in all groups treated with 0.5 U of PPE. With iNOS inhibition by AMG 1%, emphysema was attenuated. Furthermore, the proteolytic stimulus by PPE enhanced expression of nitrotyrosine and iNOS, while the group PPE+AMG showed low expression of iNOS and nitrotyrosine. PPE stimulus also induced eNOS expression, but AMG reduced it. Our results suggest a pathway of oxidative and nitrosative stress by nitric oxide production via iNOS expression in pulmonary emphysema.