Abstract
Jungia sellowii Less. (Asteraceae) is a native plant found in Southeast Brazil used traditionally to treat inflammatory diseases. This study was conducted (1) to investigate the toxicity of the crude extract (CE) and (2) to investigate the mechanism of the anti-inflammatory action of J. sellowii L. roots. The potential acute toxicity of CE was performed by administration of only different doses of CE (500, 1,000, and 2,000 i.p.) on mice for 14 days. The anti-inflammatory effect was evaluated using carrageenan-induced acute pleural cavity inflammation in a mouse model, evaluated through the following inflammatory variables: leukocyte, protein concentrations of the exudate, myeloperoxidase (MPO), adenosine deaminase (ADA), nitric oxide metabolites (NOx), and proinflammatory cytokine (tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin- (IL-) 6, and IL-12) levels in mouse pleural fluid leakage. The p65 protein phosphorylation of nuclear factor NF-kappa B (p65 NF-κB) and p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation were analyzed in lung tissue. Our results demonstrated that the administration of CE up to 2,000 mg/kg did not present a toxic effect. In addition, the pretreatment of mice with CE; its derived fractions (aqueous fraction (AqF), butanol fraction (BuOHF), and ethyl acetate fraction (EtOAcF)); and isolated compounds (curcuhydroquinone O-β-glucose (CUR) and α and β piptizol (Pip)) reduced the following inflammatory variables: neutrophils, protein concentrations of the exudate, MPO, ADA, NOx, and proinflammatory cytokine (TNF-α, IFN-γ, IL-6, and IL-12) levels in mouse pleural fluid leakage. The compounds CUR and Pip also decreased the p65 protein phosphorylation of NF-kappa B and p38 (MAPK) in lung tissue. J. sellowii L. has important anti-inflammatory activity with potential applications in drug development against inflammatory disorders. These effects found can be attributed to the ability of the new isolated compounds CUR and Pip to suppress p65 NF-κB and p-p38 MAPK pathways.
Highlights
The control of mediators released in the inflammatory process ensures the anti-inflammatory effectiveness
We evaluated the mechanism of the antiinflammatory action of the crude extract (CE), its derived fractions, and isolated compounds by evaluating several proinflammatory variables such as leukocyte influx, protein concentrations of the exudate, myeloperoxidase and adenosine deaminase, nitric oxide metabolite (NOx) levels, and Th1 polarization immune response through analysis of the level of proinflammatory cytokines: tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin- (IL-) 6, and IL-12 cytokines
Based on these previous studies that do not report evidence of toxicity, we evaluated the effect of CE, fractions obtained from CE (AqF, BuOHF, EtOAcF, HEX-F, and DMC-F), and isolated compounds (CUR and Pip) on the levels of several proinflammatory mediators to investigate the anti-inflammatory mechanism of action of J. sellowii L. using a typical mouse model of pleurisy induced by carrageenan
Summary
The control of mediators released in the inflammatory process ensures the anti-inflammatory effectiveness. The mouse model of pleurisy induced by carrageenan (Cg) is a well-characterized inflammation model which allows the quantification of different proinflammatory mediators released into the pleural fluid leakage of the pleural. Mediators of Inflammation cavity [3] This model is characterized by infiltration of neutrophils 4 h after pleurisy induction, followed by lung injury by reactive oxygen species (ROS) and reactive nitrogen species (RNS) released from active neutrophils such as hydrogen peroxide (H2O2), superoxide anion (O2−), hydroxyl radical (OH−), and peroxynitrite (ONOO−) [4]. A broad spectrum of anti-inflammatory drugs is currently available, a new strategy for the identification of new targets and discovery of new molecules, to treat diseases resistant to conventional treatment with an inflammatory nature, must be done [5, 6].
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