Systemic Administration of Calea pinnatifida Inhibits Inflammation Induced by Carrageenan in a Murine Model of Pulmonary Neutrophilia. (25th January 2020)
- Record Type:
- Journal Article
- Title:
- Systemic Administration of Calea pinnatifida Inhibits Inflammation Induced by Carrageenan in a Murine Model of Pulmonary Neutrophilia. (25th January 2020)
- Main Title:
- Systemic Administration of Calea pinnatifida Inhibits Inflammation Induced by Carrageenan in a Murine Model of Pulmonary Neutrophilia
- Authors:
- de Campos Facchin, Bruno Matheus
da Rosa, Julia Salvan
Luz, Ana Beatriz Gobbo
Moon, Yeo Jim Kinoshita
de Lima, Tamires Cardoso
Casoti, Rosana
Biavatti, Maique Weber
Dalmarco, Eduardo Monguilhott
Fröde, Tânia Silvia - Other Names:
- Sipert Carla Academic Editor.
- Abstract:
- Abstract : Objective . The aim of this study was to investigate the anti-inflammatory effects of the crude extract (CE), derived fraction, and isolated compounds from Calea pinnatifida leaves in a mouse model of pulmonary neutrophilia. Methods . The CE and derived fractions, hexane, ethyl acetate, and methanol, were obtained from C . pinnatifida leaves. The compounds 3, 5- and 4, 5-di- O - E -caffeoylquinic acids were isolated from the EtOAc fraction using chromatography and were identified using infrared spectroscopic data and nuclear magnetic resonance ( 1 H and 13 C NMR). Leukocytes count, protein concentration of the exudate, myeloperoxidase (MPO) and adenosine deaminase (ADA), and nitrate/nitrite (NO x ), tumor necrosis factor-alpha (TNF- α ), interleukin-1-beta (IL-1 β ), and interleukin-17A (IL-17A) levels were determined in the pleural fluid leakage after 4 h of pleurisy induction. We also analyzed the effects of isolated compounds on the phosphorylation of both p65 and p38 in the lung tissue. Results . The CE, its fractions, and isolated compounds inhibited leukocyte activation, protein concentration of the exudate, and MPO, ADA, NO x, TNF- α, IL-1 β, and IL-17A levels. 3, 5- and 4, 5-di- O - E -caffeoylquinic acids also inhibited phosphorylation of both p65 and p38 (P < 0.05 ). Conclusion . This study demonstrated that C . pinnatifida presents important anti-inflammatory properties by inhibiting activated leukocytes and protein concentration of the exudate. TheseAbstract : Objective . The aim of this study was to investigate the anti-inflammatory effects of the crude extract (CE), derived fraction, and isolated compounds from Calea pinnatifida leaves in a mouse model of pulmonary neutrophilia. Methods . The CE and derived fractions, hexane, ethyl acetate, and methanol, were obtained from C . pinnatifida leaves. The compounds 3, 5- and 4, 5-di- O - E -caffeoylquinic acids were isolated from the EtOAc fraction using chromatography and were identified using infrared spectroscopic data and nuclear magnetic resonance ( 1 H and 13 C NMR). Leukocytes count, protein concentration of the exudate, myeloperoxidase (MPO) and adenosine deaminase (ADA), and nitrate/nitrite (NO x ), tumor necrosis factor-alpha (TNF- α ), interleukin-1-beta (IL-1 β ), and interleukin-17A (IL-17A) levels were determined in the pleural fluid leakage after 4 h of pleurisy induction. We also analyzed the effects of isolated compounds on the phosphorylation of both p65 and p38 in the lung tissue. Results . The CE, its fractions, and isolated compounds inhibited leukocyte activation, protein concentration of the exudate, and MPO, ADA, NO x, TNF- α, IL-1 β, and IL-17A levels. 3, 5- and 4, 5-di- O - E -caffeoylquinic acids also inhibited phosphorylation of both p65 and p38 (P < 0.05 ). Conclusion . This study demonstrated that C . pinnatifida presents important anti-inflammatory properties by inhibiting activated leukocytes and protein concentration of the exudate. These effects were related to the inhibition of proinflammatory mediators. The dicaffeoylquinic acids may be partially responsible for these anti-inflammatory properties through the inhibition of nuclear transcription factor kappa B and mitogen-activated protein kinase pathways. … (more)
- Is Part Of:
- Mediators of inflammation. Volume 2020(2020)
- Journal:
- Mediators of inflammation
- Issue:
- Volume 2020(2020)
- Issue Display:
- Volume 2020, Issue 2020 (2020)
- Year:
- 2020
- Volume:
- 2020
- Issue:
- 2020
- Issue Sort Value:
- 2020-2020-2020-0000
- Page Start:
- Page End:
- Publication Date:
- 2020-01-25
- Subjects:
- Inflammation -- Mediators -- Periodicals
Biological response modifiers -- Periodicals
Inflammation (Pathologie) -- Médiateurs
Immunomodulateurs
Biological response modifiers
Inflammation -- Mediators
Immunology
Autacoids
Immunologic Factors
Cell Adhesion Molecules
Cell Communication
Cytokines
Inflammation
Periodicals
Electronic journals
616.0473 - Journal URLs:
- https://www.hindawi.com/journals/mi/ ↗
- DOI:
- 10.1155/2020/4620251 ↗
- Languages:
- English
- ISSNs:
- 0962-9351
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 12756.xml