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Updated: Dec 20, 2025

In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
Folium Sennae and emodin reverse airway smooth muscle contraction
Jun-Ying Qiu1, Li-Qun Ma1, Bei-Bei Liu1
1Hubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area and Hubei Medical Biology International Science and Technology Cooperation Base, Institute for Medical Biology, College of Life Sciences, South-Central University for Nationalities, Wuhan, China.
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 Ca2+ channels, LVDCCs), YM-58483 (a selective inhibitor of store-operated Ca2+ entry, SOCE), as well as Y-27632 (an inhibitor of Rho-associated protein kinase). In addition, LVDCC- and SOCE-mediated currents and cytosolic Ca2+ 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 Ca2+ sensitization. These findings suggest that Folium Sennae and emodin may be new sources of bronchodilators.
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