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. 2020 Oct 28:10:125.
doi: 10.1186/s13578-020-00470-8. eCollection 2020.

Dandelion extract relaxes mouse airway smooth muscle by blocking VDLCC and NSCC channels

Ping Zhao  1   2 , Jia Liu  1 , Qian Ming  1 , Di Tian  1 , Jingwen He  1 , Ziwei Yang  1 , Jinhua Shen  1 , Qing-Hua Liu  1 , Xinzhou Yang  3   4
Affiliations

Dandelion extract relaxes mouse airway smooth muscle by blocking VDLCC and NSCC channels

Ping Zhao et al. Cell Biosci. .

Abstract

Background: Asthma is one of the main intractable diseases recognized by the international medical community. The current widely used bronchodilators for asthma-β2-adrenal receptor agonists-have limited therapeutic effects, necessitating the development of novel antiasthma drugs with increased efficacy and fewer adverse effects. In this study, we investigated the relaxant effects and underlying mechanism of an ethyl acetate extract from dandelion (EAED) on mouse airway smooth muscle.

Methods: The effects of EAED on agonist-induced precontraction in mouse airway smooth muscle were evaluated with force measurement. Mouse lung slices were used to study the effects of EAED on bronchial smooth muscle. The intracellular Ca2+ concentration was measured using a calcium imaging system. L-type voltage-dependent calcium channel (VDLCC) and non-selective cationic channel (NSCC) currents were measured by patch-clamp. The lung functions of healthy and asthmatic mouse groups were assessed via the forced oscillation technique.

Results: EAED inhibits acetylcholine-induced sustained contractions of whole airway smooth muscle by inhibiting VDLCCs, NSCCs, and some unknown channels, reduces the agonist-induced increase in the cytosolic free Ca2+ concentration in airway smooth muscle cells, blocks VDLCC and NSCC currents, and relieves the respiratory resistance of healthy and asthmatic mice.

Conclusions: EAED may have potential beneficial effects on mitigating asthma attacks.

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Conflict of interest statement

Competing interestsThe authors declare no competing interests.

Figures

Fig. 1
Fig. 1
EAED inhibited high K+-induced tracheal ring contraction. a K+ (80 mM) induced a sustained contraction in mouse TR, which was blocked by EAED in a concentration-dependent manner. The dose-inhibition curve is presented. b Similar experiments were performed with vehicle (PSS containing 3% DMSO) as control. c The dose-inhibition curve is presented. The IC50 of EAED was 0.063 ± 0.005 mg/mL. The data were obtained from 7 TRs
Fig. 2
Fig. 2
Contraction induced by ACH was inhibited by cumulative addition of EAED
Fig. 3
Fig. 3
EAED inhibits contraction in lung slices
Fig. 4
Fig. 4
Nifedipine, Pyr3 partially inhibits ACH-induced contraction, respectively
Fig. 5
Fig. 5
EAED blocks high K+-evoked Ca2+ influx and ACH-elicited Ca2+ influx and Ca2+ release
Fig. 6
Fig. 6
EAED inhibits high K+ and ACH-induced Ca2+ increases in single tracheal smooth muscle cells
Fig. 7
Fig. 7
EAED blocks VDLCCs and NSCCs currents
Fig. 8
Fig. 8
The tracheal rings could still be stimulated to shrink after relaxation by EAED
Fig. 9
Fig. 9
EAED reduced the respiratory resistance induced by ACH in the control group and the asthma group
See this image and copyright information in PMC

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