1. A Plant Proteinase Inhibitor from Enterolobium contortisiliquum Attenuates Pulmonary Mechanics, Inflammation and Remodeling Induced by Elastase in Mice.
- Author
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Theodoro-Júnior OA, Righetti RF, Almeida-Reis R, Martins-Oliveira BT, Oliva LV, Prado CM, Saraiva-Romanholo BM, Leick EA, Pinheiro NM, Lobo YA, Martins MA, Oliva ML, and Tibério IF
- Subjects
- Animals, Biomarkers, Bronchoalveolar Lavage Fluid, Disease Models, Animal, Extracellular Matrix metabolism, Male, Mice, Mucins biosynthesis, Oxidative Stress, Pneumonia drug therapy, Pneumonia pathology, Airway Remodeling drug effects, Fabaceae chemistry, Pancreatic Elastase metabolism, Plant Extracts pharmacology, Pneumonia metabolism, Pneumonia physiopathology, Protease Inhibitors pharmacology
- Abstract
Proteinase inhibitors have been associated with anti-inflammatory and antioxidant activities and may represent a potential therapeutic treatment for emphysema. Our aim was to evaluate the effects of a plant Kunitz proteinase inhibitor, Enterolobium contortisiliquum trypsin inhibitor (EcTI), on several aspects of experimental elastase-induced pulmonary inflammation in mice. C57/Bl6 mice were intratracheally administered elastase (ELA) or saline (SAL) and were treated intraperitoneally with EcTI (ELA-EcTI, SAL-EcTI) on days 1, 14 and 21. On day 28, pulmonary mechanics, exhaled nitric oxide (ENO) and number leucocytes in the bronchoalveolar lavage fluid (BALF) were evaluated. Subsequently, lung immunohistochemical staining was submitted to morphometry. EcTI treatment reduced responses of the mechanical respiratory system, number of cells in the BALF, and reduced tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9), matrix metalloproteinase-12 (MMP-12), tissue inhibitor of matrix metalloproteinase (TIMP-1), endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS)-positive cells and volume proportion of isoprostane, collagen and elastic fibers in the airways and alveolar walls compared with the ELA group. EcTI treatment reduced elastase induced pulmonary inflammation, remodeling, oxidative stress and mechanical alterations, suggesting that this inhibitor may be a potential therapeutic tool for chronic obstructive pulmonary disease (COPD) management.
- Published
- 2017
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