cyanidin-3-o-beta-glucopyranoside and Asthma

cyanidin-3-o-beta-glucopyranoside has been researched along with Asthma* in 1 studies

Other Studies

1 other study(ies) available for cyanidin-3-o-beta-glucopyranoside and Asthma

ArticleYear
Cyanidin-3-O-β-glucoside attenuates allergic airway inflammation by modulating the IL-4Rα-STAT6 signaling pathway in a murine asthma model.
    International immunopharmacology, 2019, Volume: 69

    Cyanidin-3-O-β-glucoside (Cy-3-g), a typical and abundant monomer of anthocyanins, exhibits a variety of biological activities, such as anti-atherosclerosis, anti-obesity, and anticancer effects. However, to date little is known about its effects on asthma. This study aimed to investigate the efficacy of dietary Cy-3-g on allergic asthma in an animal model. BALB/c mice were sensitized and challenged with ovalbumin (OVA) to induce allergic asthma. The pathological changes of the lung tissues, type 2 helper (Th2)-associated cytokine production in bronchoalveolar lavage fluid (BALF), and the interleukin 4 receptor alpha (IL-4Rα)-signal transducer and activator of transcription 6 (STAT6) signaling pathway activities were assessed. We found that Cy-3-g significantly inhibited OVA-induced inflammatory cell infiltration and mucus hyper-production in lung tissues, reduced the production of interleukin 4 (IL-4), interleukin 5 (IL-5) and interleukin 13 (IL-13) in BALF. Furthermore, Cy-3-g effectively suppressed OVA-induced up-regulation of the IL-4Rα-STAT6 signaling pathway activity of the lung tissues. These results demonstrated that dietary Cy-3-g could attenuate allergic airway inflammation in a murine asthma model, and Cy-3-g might be used as an agent for asthma prevention and/or treatment in the future.

    Topics: Allergens; Animals; Anthocyanins; Anti-Inflammatory Agents; Asthma; Cytokines; Dietary Supplements; Disease Models, Animal; Female; Glucosides; Humans; Lung; Mice; Mice, Inbred BALB C; Ovalbumin; Receptors, Cell Surface; Respiratory Hypersensitivity; STAT6 Transcription Factor; Th2 Cells

2019