基础医学与临床 ›› 2023, Vol. 43 ›› Issue (11): 1648-1654.doi: 10.16352/j.issn.1001-6325.2023.11.1648

• 研究论文 • 上一篇    下一篇

没食子酸减轻香烟烟雾诱导的小鼠气道炎性反应

赵芳1*, 赵青2, 刘玮琳3, 李菲4   

  1. 河北省第八人民医院 河北省老年病医院 1.呼吸肾内科;2.医教处,河北 石家庄 050000;
    3.河北医科大学第四医院 感染性疾病科,河北 石家庄 050000;
    4.河北医科大学第一医院 保健处, 河北 石家庄 050000
  • 收稿日期:2023-04-06 修回日期:2023-07-18 出版日期:2023-11-05 发布日期:2023-10-30
  • 通讯作者: *tuteth438@21cn.com
  • 基金资助:
    2023年度河北省医学科学研究课题计划(20231194)

Gallic acid alleviates airway inflammation induced by cigarette smoke in mice

ZHAO Fang1*, ZHAO Qing2, LIU Weilin3, LI Fei4   

  1. 1. Department of Respiratory and Renal Medicine;2. Department of Medical Education, Hebei Eighth People's Hospital/Hebei Geriatrics Hospital, Shijiazhuang 050000;
    3. Department of Infectious Diseases, the Fourth Hospital of Hebei Medical University, Shijiazhuang 050000;
    4. Department of Health Care, the First Hospital of Hebei Medical University, Shijiazhuang 050000, China
  • Received:2023-04-06 Revised:2023-07-18 Online:2023-11-05 Published:2023-10-30
  • Contact: *tuteth438@21cn.com

摘要: 目的 研究没食子酸(GA)对香烟烟雾(CS)诱导的小鼠慢性阻塞性肺病(COPD)相关的肺部炎性反应的作用。方法 构建CS诱导的小鼠模型。分析支气管肺泡灌洗液中的炎性细胞的数量和促炎细胞因子的水平。相应试剂盒检测肺组织匀浆中活性氧(ROS)、谷胱甘肽(GSH)、丙二醛(MDA)和蛋白羰基的活性。Western blot分析IL-13/STAT6通路活性。结果 GA抑制SC诱导的炎性细胞浸润(中性粒细胞、淋巴细胞和巨噬细胞)和促炎细胞因子(IL-6、TNF-α和IL-1β)的水平。GA可以减轻暴露于CS的小鼠肺组织氧化还原失衡。结论 GA有效地减轻COPD模型小鼠肺部炎性反应和氧化应激。

关键词: 没食子酸, IL-13/STAT6信号通路, 慢性阻塞性肺病, 气道炎性反应

Abstract: Objective To investigate the effect of gllic acid (GA) on the pulmonary inflammatory response associated with chronic obstructive pulmonary disease (COPD) induced by cigarette smoking (CS) in mice. Methods The mouse model induced by CS was constructed. The counting number of inflammatory cells and the level of proinflammatory cytokines in bronchoalveolar lavage fluid were analyzed. The ROS, GSH, MDA and protein carbonyl activity in lung tissue homogenate were determined by commercially available kits. Western blot was used to analyze IL-13/STAT6 pathway. Results GA inhibited SC-induced inflammatory cell infiltration (neutrophils, lymphocytes, and macrophages) and decreased the level of pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β). GA alleviated the redox imbalance and CS-induced airway inflammation in lung tissue of CS exposed mice. The later might be mediated by by inhibiting IL-13/STAT6 signaling pathway. Conclusions GA effectively modulates pulmonary inflammation and oxidative stress in mice associated with COPD pathogenesis.

Key words: gallic acid, IL-13/STAT6 signaling pathway, chronic obstructive pulmonary disease, airway inflammation

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