Autor: |
Lemos, Ari Sérgio de O, Campos, Lara M, Granato, Juliana da T, Goliatt, Priscila V Z C, Dib, Paula R B, Hottz, Eugenio D, Glanzmann, Nícolas, Campos, Laíris C, Bizarro, Heloisa D S, Chedier, Luciana M, Coimbra, Elaine S, Fabri, Rodrigo L |
Předmět: |
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Zdroj: |
Journal of Pharmacy & Pharmacology; Oct2023, Vol. 75 Issue 10, p1388-1393, 6p |
Abstrakt: |
Objectives: To evaluate the ability of the aqueous extract of Mitracarpus frigidus (MFAq) to inhibit lipid body formation and inflammatory mediator production in macrophages stimulated with lipopolysaccharide (LPS) and interferon gamma (IFN-γ). Methods: MFAq was chemically characterized by ultrafast liquid chromatography/quadruple time-of-flight tandem mass spectrometry. The macrophages obtained from mice were incubated with MFAq. Cell viability and membrane integrity were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and propidium iodide assays, respectively. Moreover, NO, reactive oxygen species (ROS), transforming growth factor beta (TGF-β), prostaglandin E2 (PGE2) levels and lipid bodies (LBs) were examined in macrophages that were stimulated with LPS and IFN-γ and treated with MFAq. Finally, molecular docking analysis was conducted to investigate the interaction of MFAq with the cyclooxygenase 2 (COX-2) enzyme. Key findings: Chlorogenic acid, clarinoside, harounoside, rutin, kaempferol-3O-rutinoside and 2-azaanthraquinone were identified in MFAq. MFAq significantly inhibited NO, ROS and LBs, and did not affect the membrane integrity of macrophages. MFAq-treated cells showed significantly lower levels of TGF-β and PGE2. Molecular docking demonstrated that the compounds found in MFAq are able to inhibit COX-2 by binding to important residues in the catalytic site. Conclusions: MFAq interferes with lipid metabolism in stimulated macrophages, leading to the reduction of important inflammatory mediators. Furthermore, MFAq can directly inhibit the COX-2 enzyme or inhibit its expression owing to its ability to reduce NO production. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
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