Astragalin Inhibits Allergic Inflammation and Airway Thickening in Ovalbumin-Challenged Mice

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• 作者：Yun-Ho Kim ; Yean-Jung Choi ; Min-Kyung Kang ; Sin-Hye Park ; Lucia Dwi Antika ; Eun-Jung Lee ; Dong Yeon Kim ; Young-Hee Kang
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2017
• 出版时间：February 1, 2017
• 年：2017
• 卷：65
• 期：4
• 页码：836-845
• 全文大小：891K
• ISSN：1520-5118

文摘

Lung inflammation and oxidative stress are the major contributors to the development of obstructive pulmonary diseases. Macrophages are involved in pulmonary inflammation and alveolar damage in emphysema. Astragalin is an anti-inflammatory flavonoid present in persimmon leaves and green tea seeds. This study elucidated that astragalin inhibited inflammatory cell infiltration induced by 20 μM H₂O₂ and blocked airway thickening and alveolar emphysema induced by 20 μg of ovalbumin (OVA) in mice. OVA induced mouse pulmonary MCP-1, and H₂O₂ enhanced the expression of MCP-1/ICAM-1/αv integrin in bronchial airway epithelial BEAS-2B cells. Such induction was inhibited by supplying 10–20 mg/kg of astragalin to OVA-challenged mice and 1–20 μM astragalin to oxidant-stimulated cells. Oral administration of 20 mg/kg of astragalin reduced the induction of F4/80/CD68/CD11b in airways of mice challenged with OVA. Additionally, emphysema tissue damage was observed in OVA-exposed alveoli. Mast cell recruitment in the airway subepithelium was blocked by supplementing astragalin to OVA-challenged mice. Orally treating 20 mg/kg of astragalin reduced α-SMA induction in inflammation-occurring airways and appeared to reverse airway thickening and constriction induced by an OVA episode. These results revealed that astragalin may improve airway thickening and alveolar destruction with blockade of allergic inflammation in airways. Therefore, astragalin may be a therapeutic agent antagonizing asthma and obstructive pulmonary diseases.