1. Systemic Administration of Calea pinnatifida Inhibits Inflammation Induced by Carrageenan in a Murine Model of Pulmonary Neutrophilia.
- Author
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de Campos Facchin BM, da Rosa JS, Luz ABG, Moon YJK, de Lima TC, Casoti R, Biavatti MW, Dalmarco EM, and Fröde TS
- Subjects
- Adenosine Deaminase metabolism, Animals, Anti-Inflammatory Agents pharmacology, Carrageenan, Disease Models, Animal, Female, Inflammation chemically induced, Interleukin-17 metabolism, Interleukin-1beta metabolism, Leukocyte Disorders chemically induced, Lung drug effects, Lung metabolism, Lung pathology, Lung Diseases chemically induced, Mice, Nitrates chemistry, Nitrites chemistry, Peroxidase metabolism, Phosphorylation, Pleurisy drug therapy, Quinic Acid analogs & derivatives, Quinic Acid chemistry, Transcription Factor RelA metabolism, Tumor Necrosis Factor-alpha metabolism, p38 Mitogen-Activated Protein Kinases metabolism, Asteraceae chemistry, Inflammation drug therapy, Leukocyte Disorders drug therapy, Lung Diseases drug therapy, Neutrophils drug effects, Plant Extracts pharmacology
- 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 and13 C NMR). Leukocytes count, protein concentration of the exudate, myeloperoxidase (MPO) and adenosine deaminase (ADA), and nitrate/nitrite (NOx ), 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, NOx , 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., Competing Interests: The authors declare that they have no conflict of interest., (Copyright © 2020 Bruno Matheus de Campos Facchin et al.)- Published
- 2020
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