title: Hyperoside attenuates OVA-induced allergic airway inflammation by activating Nrf2.
abstract: Allergic airways disease (AAD) is one of the most common medical illnesses that is associated with an increased allergic airway inflammation. Hyperoside, an active compound isolated from Rhododendron brachycarpum G. Don, has been reported to have anti-inflammatory effect. The aim of this study was to analyze the protective effect of hyperoside on OVA-induced allergic airway inflammation in mice. In the present study, the mouse asthma model was induced by given OVA and hyperoside was administrated 1h before OVA challenge. The levels of IL-4, IL-5, IL-13, and IgE were detected by ELISA. H&E staining was used to assess lung histopathological changes. The expression of NF-κB p65, IκB, HO-1, and Nf-E2 related factor 2 (Nrf2) were measured by western blot analysis. The results showed that hyperoside significantly reduced the inflammatory cells infiltration and the levels of IL-4, IL-5, IL-13, and IgE. Hyperoside significantly inhibited OVA-induced oxidative stress as demonstrated by decreased MDA, and increased GSH and SOD levels. Treatment of hyperoside also inhibited OVA-induced airway hyperresponsiveness (AHR). Furthermore, the results showed that treatment of hyperoside significantly inhibited LPS-induced NF-κB activation. In addition, hyperoside was found to activate Nrf2/HO-1 signaling pathway. In conclusion, these results suggest that hyperoside ameliorates OVA-induced allergic airway inflammation by activating Nrf2 signaling pathway.
authors.affiliation: Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan 430060, China. Electronic address: yp800111@163.com.
authors.forename: Peng
authors.initials: P
authors.lastname: Ye
authors.affiliation: Pharmacy department of medical college, Wuhan University of Science and technology, Wuhan 430065, China.
authors.forename: Xi-Liang
authors.initials: XL
authors.lastname: Yang
authors.affiliation: Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan 430060, China.
authors.forename: Xing
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan 430060, China.
authors.forename: Cai
authors.initials: C
authors.lastname: Shi
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000139:chemically induced / Q000188:drug therapy*; D002478:Cells, Cultured; D016207:Cytokines / Q000097:blood; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D008168:Lung / Q000187:drug effects* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D010047:Ovalbumin / Q000276:immunology; D018384:Oxidative Stress / Q000187:drug effects; D011014:Pneumonia / Q000188:drug therapy*; D011794:Quercetin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D029793:Rhododendron / Q000276:immunology*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D018927:Anti-Asthmatic Agents; D016207:Cytokines; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; C495636:Nfe2l2 protein, mouse; D007073:Immunoglobulin E; C021304:hyperoside; D010047:Ovalbumin; D011794:Quercetin
keywords: Asthma; HO-1; Hyperoside; Nrf2; OVA