Astragalin Attenuates Allergic Inflammation in a Murine Asthma Model
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Astragalin Attenuates Allergic Inflammation in a Murine Asthma Model Jiping Liu,1 Yue Cheng,1 Xiaoshuang Zhang,1 Xue Zhang,1 Shuxian Chen,1 Zongmiao Hu,1 Chunmei Zhou,1 Enhu Zhang,1,3 and Shiping Ma2,3
Abstract—The present study aimed to determine the protective effects and the underlying mechanisms of astragalin (AG) on ovalbumin (OVA)-induced allergic inflammation in a mouse model of allergic asthma. Our study demonstrated that AG inhibited OVA-induced increases in eosinophil count; IL-4, IL5, IL-13, and IgE were recovered in bronchoalveolar lavage fluid, and increased IFN-γ level in bronchoalveolar lavage fluid. Histological studies demonstrated that AG substantially inhibited OVAinduced eosinophilia in lung tissue. Western blot analysis demonstrated that AG treatments markedly inhibited OVA-induced SOCS-3 expression and enhancement of SOCS-5 expression in an asthma model. Our findings support the possible use of AG as a therapeutic drug for patients with allergic asthma. KEY WORDS: astragalin; allergic inflammation; suppressor of cytokine signaling.
INTRODUCTION Asthma is a chronic inflammatory disease of the lung that is characterized by heightened sensitivity to stimuli that induce bronchoconstriction (airway hyperresponsiveness or AHR), marked tissue eosinophilia, increased mucus production due to the increased differentiation of bronchial epithelium into mucus-producing goblet cells, and prominent structural changes in the airways. These structural changes, which are collectively referred to as airway remodeling, include airway sub-epithelial fibrosis and myofibroblast hyperplasia [1, 2]. Type 1 allergies, which play critical roles in the pathogenesis of asthma, are caused by characteristic immune responses to allergens, primarily mediated by Th2 cells. Th2 cells synthesize high levels of interleukin (IL)-4, IL-5, and IL-13, which leads to the production of allergen1
Department of Pharmacology, Shaanxi University of Chinese Medicine, Xianyang, China712046 2 Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China210009 3 To whom correspondence should be addressed to Enhu Zhang at Department of Pharmacology, Shaanxi University of Chinese Medicine, Xianyang, China712046. E-mail: [email protected]; and Shiping Ma at Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China210009. E-mail: [email protected]
specific immunoglobulin (Ig) E and the release of mediators from mast cells [3]. Th2 cells produce a distinct set of cytokines that are necessary for the allergic response. These include the cytokines IL-4 and IL-13, which promote IgE production; IL-5 and granulocyte macrophage-colonystimulating factor (GM-CSF), which promote eosinophil production in the bone marrow; and IL-10, which promotes B cell differentiation into plasma cells. By contrast, Th2 cells do not produce IL-2 and interferon-g. These cytokines are characteristic of Th1 cells, which reciprocally do not produce Th2-type cytokines. Thus, interventions that i
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