RT Journal Article
SR Electronic
T1 Plant proteinase inhibitor from <em>Enterolobium contortisiliquum</em> (<em>EcTI</em>) attenuates elastase-induced pulmonary inflammatory, remodeling and mechanical alterations in mice
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P828
VO 40
IS Suppl 56
A1 Osmar A. Theodoro-Junior
A1 Ricardo Henrique Marques
A1 Rafael Almeida-Reis
A1 Bruno T. Martins-Oliveira
A1 Leandro V. Oliva
A1 Tales Lopes
A1 Carla M. Prado
A1 Maria L.V. Oliva
A1 Milton Martins
A1 Iolanda F.L.C. Tibério
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/P828.abstract
AB Aims: to evaluate if a plant Kunitz proteinase inhibitor EcTI contributes to inactivation of elastase-induced mechanical, inflammatory and remodelling alterations. Methods: C57Bl6 mice received elastase (E group). Control group received saline (Ve group). Mice were treated with EcTI (2mg/kg) on days 1, 14 and 21 after elastase instillation (I-E group). On day 30, mice were anesthetized, mechanically ventilated and we analyzed respiratory system resistance (Rrs) and elastance (Ers), tissue elastance (Htis), tissue damping (Gtis), airway resistance (Raw) and exhaled nitric oxide (ENO). Bronchoalveolar lavage fluid (BALF) was performed, lungs were removed and by morphometry, we quantified the mean linear intercept (Lm), collagen and elastic fibers in lung parenchyma. Results: In E-group there was a significant increase in the Ers, Rrs, Raw, Htis, Lm, ENO, total cells and macrophages,neutrophils and lymphocytes in BALF, elastic and collagen fibres compared to controls (p&lt;0.05). In I-E group there was a decreased in Lm (57.63±5.2µm), Raw (0.29±0.05cmH2O/ml/s), Ers (34.71±3.16cmH2O/L), Htis (36.30±4.42cmH2O/mL/s), macrophages (94.86±2.36%), neutrophils (3.29±2.31%), and lymphocytes (0.91±0.28%) in the BALF, ENO (31.67±2.23ppb) and collagen fibers (0.69%±0.04%) compared to E-group (p&lt;0.05). Conclusions: This proteinase inhibitor (EcTI) reduced elastase-induced pulmonary inflammatory, remodeling and mechanical alterations induced by elastase. Although more studies need to be performed, this inhibitor may contribute as potential therapeutic tool for COPD management. Financial Support: FAPESP, CNPq, LIM-20 HCFMUSP.