The Antidiabetic Agent Glibenclamide Protects Airway Hyperresponsiveness and Inflammation in Mice

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• 作者：Wei Cui (1)
  Shufang Zhang (2)
  Zhijian Cai (3)
  Xinlei Hu (2)
  Ruifeng Zhang (4)
  Yong Wang (5)
  Na Li (1)
  Zhihua Chen (6)
  Gensheng Zhang (1)
  
  1. Department of Critical Care Medicine ; Second Affiliated Hospital ; Zhejiang University School of Medicine ; Hangzhou ; 310009 ; China
  2. Binjiang Branch ; Second Affiliated Hospital ; Zhejiang University School of Medicine ; Hangzhou ; 310009 ; China
  3. Department of Immunology ; Zhejiang University ; Hangzhou ; Zhejiang ; 310009 ; China
  4. Department of Respiratory Medicine of Sir Run Run Shaw Hospital ; Zhejiang University School of Medicine ; Hangzhou ; Zhejiang ; 310009 ; China
  5. Department of General Surgery ; Ningbo First Hospital ; Ningbo ; Zhejiang ; 315010 ; China
  6. Department of Respiratory and Critical Care Medicine ; Second Affiliated Hospital ; Zhejiang University School of Medicine ; Hangzhou ; Zhejiang ; 310009 ; China
  
• 关键词：airway hyperresponsiveness ; airway inflammation ; asthma ; glibenclamide ; sulfonylurea receptor 1
• 刊名：Inflammation
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：38
• 期：2
• 页码：835-845
• 全文大小：3,142 KB
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• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

Glibenclamide has a newly discovered role in inflammation regulation besides its antidiabetic effect. As an inhibitor of ATP-sensitive potassium (KATP) channel, glibenclamide antagonizes the relaxation of the tracheal smooth muscle. This indicates that glibenclamide might attenuate airway inflammation while aggravate airway hyperresponsiveness (AHR) in asthmatics. Clinically, many diabetics with asthma are prescribed with glibenclamide to control blood glucose. However, whether glibenclamide could exert any effects on asthmatic inflammation remains unknown. Using an ovalbumin (OVA)-induced mouse model of asthma, we evaluated the effects of glibenclamide on the AHR and inflammation. Interestingly, glibenclamide reduced all the cardinal features of asthma in OVA-challenged mice, including AHR, airway inflammation, and T-helper type 2 (Th2) cytokines. Glibenclamide also downregulated OVA-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and phosphorylated signal transducer and activator of transcription 6 (p-STAT6) in the lung. In addition, increased sulfonylurea receptor 1 (SUR1) expression in the lung was observed after the OVA challenge. These findings suggest that the classic sulfonylurea glibenclamide plays an important protective role in the development of asthma, which not only provides the evidence for the safety of prescribed glibenclamide in diabetics combined with asthma but also indicates a possible new therapeutic for asthma via targeting glibenclamide-related pathways.