Literature DB >> 35658632

Isoorientin ameliorates OVA-induced asthma in a murine model of asthma.

Shuai Liang1, Yuanyuan Zhao1, Guozhen Chen1, Chunxiao Wang1.   

Abstract

Allergic asthma which is induced by ovalbumin (OVA) is a chronic airway inflammation disease. Isoorientin (Iso) is a natural C-glucosyl flavone with many biological properties. We aimed to evaluate the effectiveness of Iso on OVA-induced allergic asthma. A total of 30 C57BL/6 mice were randomly divided into five groups: control group, OVA group, Dex (dexamethasone, 10 mg/kg) group, low-dose Iso group (Iso-L, 25 mg/kg), and high-dose Iso group (Iso-H, 50 mg/kg). The serum and bronchoalveolar lavage fluid (BALF) were collected for biochemical parameters, the lung tissue was collected for hematoxylin-eosin (H&E) staining, immunohistochemistry (IHC), and western blot. The levels of IL-4, IL-5, IL-13, malondialdehyde (MDA), NO, and reactive oxygen species (ROS) in Iso-L and Iso-H groups were significantly lower than that in model group (p < 0.05). Simultaneously, the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity were higher than that in model group (p < 0.05). Iso significantly ameliorated airway hyperresponsiveness. Meanwhile, H&E staining revealed that mice treated with Iso resulted in the ameliorated inflammatory cell infiltration and a reduction in interstitial thickening. The nuclear factor erythroid 2-like 2 (Nrf2) and HO-1 protein expression in Iso-L and Iso-H groups were enhanced over that in model group, while p-NF-κB-p65 and p-IκB-α protein expression was decreased (p < 0.05). Our research indicated that Iso alleviated the OVA-induced allergic asthma, and this effect can be explained by the modulation of Nrf2/HO-1 and NF-κB signaling pathway; thus, the results providing a therapeutic rationale for the treatment of Iso on allergic asthma.

Entities:  

Keywords:  Hyperresponsiveness; Nrf2/HO-1 signaling; dexamethasone; histopathological; inflammation; oxidative stress

Mesh:

Substances:

Year:  2022        PMID: 35658632      PMCID: PMC9493767          DOI: 10.1177/15353702221094505

Source DB:  PubMed          Journal:  Exp Biol Med (Maywood)        ISSN: 1535-3699


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