Folium Sennae and emodin reverse airway smooth muscle contraction. (29th May 2020)

• Record Type: Journal Article
• Authors: Qiu, Jun‐Ying; Ma, Li‐Qun; Liu, Bei‐Bei; Zhang, Wen‐Jing; Liu, Meng‐Su; Wang, Ge‐Ge; Zhao, Xiao‐Xue; Luo, Xi; Wang, Qian; Xu, Hao; Zang, Dun‐An; Shen, Jinhua; Peng, Yong‐Bo; Zhao, Ping; Xue, Lu; Yu, Meng‐Fei; Chen, Weiwei; Dai, Jiapei; Liu, Qing‐Hua
• Is Part Of: Cell biology international. Volume 44:Number 9(2020)
• Page Start: 1870
• Page End: 1880
• Publication Date: 2020-05-29
• Subjects: Ca2+ sensitization -- emodin -- Folium Sennae -- L‐type voltage‐dependent Ca2+ channels -- respiratory system resistance -- store‐operated Ca2+ entry; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.11393
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: The objective of this project was to find a bronchodilatory compound from herbs and clarify the mechanism. We found that the ethanol extract of Folium Sennae (EEFS) can relax airway smooth muscle (ASM). EEFS inhibited ASM contraction, induced by acetylcholine, in mouse tracheal rings and lung slices. High‐performance liquid chromatography assay showed that EEFS contained emodin. Emodin had a similar reversal action. Acetylcholine‐evoked contraction was also partially reduced by nifedipine (a selective inhibitor of L‐type voltage‐dependent Ca 2+ channels, LVDCCs), YM‐58483 (a selective inhibitor of store‐operated Ca 2+ entry, SOCE), as well as Y‐27632 (an inhibitor of Rho‐associated protein kinase). In addition, LVDCC‐ and SOCE‐mediated currents and cytosolic Ca 2+ elevations were inhibited by emodin. Emodin reversed acetylcholine‐caused increases in phosphorylation of myosin phosphatase target subunit 1. Furthermore, emodin, in vivo, inhibited acetylcholine‐induced respiratory system resistance in mice. These results indicate that EEFS‐induced relaxation results from emodin inhibiting LVDCC, SOCE, and Ca 2+ sensitization. These findings suggest that Folium Sennae and emodin may be new sources of bronchodilators.