ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
The anti-asthma herbal medicine ASHMI acutely inhibits airway smooth muscle contraction via prostaglandin E2 activation of EP2/EP4 receptors.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The inhibition of pathological IgE in allergic diseases by natural compounds.Natural products and bioprospecting · 2026Review
- Physician attitudes toward natural syrup formulations for cough and sore throat: a multinational cross-sectional survey of 398 healthcare professionals across 13 countries.Frontiers in pharmacology · 2026Article
- Natural Products for Drug Discovery in the 21st Century: Innovations for Novel Drug Discovery.International journal of molecular sciences · 2018Review
- Immune Homeostasis: Effects of Chinese Herbal Formulae and Herb-Derived Compounds on Allergic Asthma in Different Experimental Models.Chinese journal of integrative medicine · 2018Review
- A snake venom group IIA PLAScientific reports · 2017Article
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Traditional Chinese medicine for treatment of liver diseases: progress, challenges and opportunities.Journal of integrative medicine · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Our previous studies have shown that the anti-asthma traditional Chinese medicine herbal formula ASHMI (anti-asthma simplified herbal medicine intervention) inhibits acetylcholine-induced contractions of tracheal rings from ovalbumin-sensitized and naive mice in a β-adrenoceptor-independent manner. We sought to determine whether acute in vivo ASHMI administration inhibits airway hyperreactivity (AHR) in a murine model of allergic asthma and acetylcholine-induced tracheal ring constriction ex vivo and to elucidate the cellular mechanisms underlying these effects. Ovalbumin-sensitized mice received a single oral ASHMI dose 2 h before intravenous acetylcholine challenge. AHR was determined by invasive airway measurements. Myography was used to determine the effects of ASHMI on acetylcholine-induced constriction of tracheal rings from asthmatic mice with or without epithelial denudation. The effect of cyclooxygenase inhibition and EP2/EP4 receptor blockade on ASHMI attenuation of acetylcholine contractions was evaluated. Tracheal cAMP and PGE2 levels were measured by ELISA. A single acute oral dose of ASHMI dramatically reduced AHR in response to acetylcholine provocation in ovalbumin-sensitized mice (P < 0.001). In ex vivo experiments, ASHMI significantly and dose-dependently reduced tracheal ring constriction to acetylcholine (P < 0.05-0.001), which was epithelium independent and associated with elevated cAMP levels. This effect was abrogated by cyclooxygenase inhibition or EP2/EP4 receptor blockade. ASHMI also inhibited contraction to high K(+) (P < 0.001). ASHMI increased tracheal ring PGE2 release in response to acetylcholine or high K(+) (P < 0.05 for both). ASHMI produced direct and acute inhibition of AHR in vivo and blocked acetylcholine-induced tracheal ring constriction via the EP2/EP4 receptor pathway, identifying the mechanism by which ASHMI is an orally active bronchoprotective agent.
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