京尼平苷酸通过抑制过敏性气道炎症和调节肠道菌群抑制OVA诱导的哮喘
2025/04/06
摘要
背景：哮喘是一种严重的慢性呼吸系统炎症性疾病。
目的：本研究旨在探讨京尼平苷酸（GPA）在卵清蛋白（OVA）诱导的小鼠哮喘中的作用，并阐明其潜在机制。
方法：将小鼠分为对照组、OVA组、OVA+GPA（12.5、25、50 mg/kg）组。通过ELISA检测炎症介质，通过16S RNA测序检测肠道菌群。
结果：结果表明，GPA减轻了OVA诱导的肺损伤、炎症细胞浸润和黏液分泌过多。GPA还抑制了OVA诱导的IL-4、IL-5、IL-13和IgE的产生，并增加了IFN-γ的产生。此外，GPA抑制了OVA诱导的NF-κB活化并增加了Nrf2的表达。同时，GPA缓解了OVA诱导的肠道菌群失调。经过GPA治疗后，哮喘小鼠肠道菌群的多样性和丰度增加。在门水平上，GPA显著降低了Ligilactobacillus、Lachnospiraceae、Helicobacter和Bacteroidales的相对丰度，并显著增加了Muribaculaceae和Muribaculum的相对丰度。
结论：综上所述，GPA通过抑制炎症和调节肠道菌群保护小鼠免受OVA诱导的哮喘。
Geniposidic acid inhibits OVA-induced asthma by suppressing allergic airway inflammation and regulating gut microbiota.
Yang, Zheng; Dengyu, Gao;
Abstrast
Background: Asthma is a serious chronic inflammatory disease of the respiratory system.
Objective: In this study, we aimed to explore the role of geniposidic acid (GPA) in ovalbumin (OVA)-induced asthma in mice and to clarify its underlying mechanism.
Methods: The mice were divided into control group, OVA group, OVA+GPA (12.5, 25, 50 mg/kg) groups. Inflammatory mediators were measured by ELISA. Gut microbiota was detected by 16S RNA sequencing.
Results:The results demonstrated that GPA attenuated OVA-induced lung injury, inflammatory cell infiltration, and mucus hypersecretion. OVA-induced IL-4, IL-5, IL-13, and IgE production was also inhibited by GPA. IFN-γ production was increased by GPA. Furthermore, GPA inhibited OVA-induced NF-κB activation and increased Nrf2 expression. In addition, GPA alleviated the dysbiosis of gut microbiota induced by OVA. After GPA treatment, the diversity and abundance of intestinal microbiota in asthma mice increased. At the phylum level, GPA significantly reduced the relative abundance of Ligilactobacillus, Lachnospiraceae, Helicobacter, and Bacteroidales and significantly increased the relative abundance of Muribaculaceae and Muribaculum.
Conclusions: In conclusion, GPA protect mice against OVA-induced asthma through suppressing inflammation and regulating gut microbiota.
背景：哮喘是一种严重的慢性呼吸系统炎症性疾病。
目的：本研究旨在探讨京尼平苷酸（GPA）在卵清蛋白（OVA）诱导的小鼠哮喘中的作用，并阐明其潜在机制。
方法：将小鼠分为对照组、OVA组、OVA+GPA（12.5、25、50 mg/kg）组。通过ELISA检测炎症介质，通过16S RNA测序检测肠道菌群。
结果：结果表明，GPA减轻了OVA诱导的肺损伤、炎症细胞浸润和黏液分泌过多。GPA还抑制了OVA诱导的IL-4、IL-5、IL-13和IgE的产生，并增加了IFN-γ的产生。此外，GPA抑制了OVA诱导的NF-κB活化并增加了Nrf2的表达。同时，GPA缓解了OVA诱导的肠道菌群失调。经过GPA治疗后，哮喘小鼠肠道菌群的多样性和丰度增加。在门水平上，GPA显著降低了Ligilactobacillus、Lachnospiraceae、Helicobacter和Bacteroidales的相对丰度，并显著增加了Muribaculaceae和Muribaculum的相对丰度。
结论：综上所述，GPA通过抑制炎症和调节肠道菌群保护小鼠免受OVA诱导的哮喘。
（中日友好医院呼吸与危重症医学科 万静萱 摘译 林江涛 审校）
（Front Immunol 2025;16(0):1549459 DOI: 10.3389/fimmu.2025.1549459.IF:5.085）
Geniposidic acid inhibits OVA-induced asthma by suppressing allergic airway inflammation and regulating gut microbiota.
Yang, Zheng; Dengyu, Gao;
Abstrast
Background: Asthma is a serious chronic inflammatory disease of the respiratory system.
Objective: In this study, we aimed to explore the role of geniposidic acid (GPA) in ovalbumin (OVA)-induced asthma in mice and to clarify its underlying mechanism.
Methods: The mice were divided into control group, OVA group, OVA+GPA (12.5, 25, 50 mg/kg) groups. Inflammatory mediators were measured by ELISA. Gut microbiota was detected by 16S RNA sequencing.
Results:The results demonstrated that GPA attenuated OVA-induced lung injury, inflammatory cell infiltration, and mucus hypersecretion. OVA-induced IL-4, IL-5, IL-13, and IgE production was also inhibited by GPA. IFN-γ production was increased by GPA. Furthermore, GPA inhibited OVA-induced NF-κB activation and increased Nrf2 expression. In addition, GPA alleviated the dysbiosis of gut microbiota induced by OVA. After GPA treatment, the diversity and abundance of intestinal microbiota in asthma mice increased. At the phylum level, GPA significantly reduced the relative abundance of Ligilactobacillus, Lachnospiraceae, Helicobacter, and Bacteroidales and significantly increased the relative abundance of Muribaculaceae and Muribaculum.
Conclusions: In conclusion, GPA protect mice against OVA-induced asthma through suppressing inflammation and regulating gut microbiota.
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