Résumé
Aim To investigate the effect of astragalin (AG) on airway inflammation in asthmatic mice and its mechanism. Methods Fifty SPF male mice were randomly divided into normal group, asthma model group, and astragalin low (AG25), medium (AG50), and high (AG100) dose groups. A mouse model of asthma was prepared by egg albumin inhalation, the number of cells was counted by Diff-Quik staining after collecting bronchoalveolar lavage fluid (BALF), and IL4, 5, and 13 levels in BALF were measured by ELISA. The inflammatory changes in mouse lung tissues were observed using HE staining. Reactive oxygen species (ROS) levels were measured using a DCFH-DA probe, and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured by colorimetry. IL-4, IL-5, IL-13, NOX2, p47phox, p-NF-κBp65, NF-κBp65, IκBα, p-IκBα and β-actin expressions in lung tissues were detected by Western blot. Results AG significantly reduced the number of inflammatory cells and total cells in BALF, decreased IL-4, IL-5, and IL-13 contents in BALF and lung tissues, and reduced inflammatory cell infiltration in lung tissues. AG inhibited nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) and p47phox expression, decreased ROS levels and MDA levels, increased SOD activity, and inhibited IκBα and NF-κBp65 phosphorylation. Conclusion AG attenuates airway inflammation in asthma by modulating the oxidative stress response through the NOX2/ROS/NF-κB signaling pathway.