Characteristics of evodiamine-exerted stimulatory effects on rat jejunal contractility

This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted...

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Published inNatural product research Vol. 29; no. 4; pp. 388 - 391
Main Authors Xiong, Yong-Jian, Chen, Da-Peng, Peng, Jin-Yong, Wang, Jing-Yu, Lv, Bo-Chao, Liu, Fang-Fei, Lin, Yuan
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 16.02.2015
Subjects
acetylcholine
Animals
antagonists
atropine
calcium
Calcium - metabolism
Calcium Channel Blockers - pharmacology
cholinergic nervous
Evodia rutaecarpa
evodiamine
Gastrointestinal Motility - drug effects
jejunal contractility
jejunum
Jejunum - drug effects
Molecular Structure
Muscle Contraction - drug effects
myosin
Myosins - metabolism
neurons
Nifedipine - pharmacology
Phosphorylation
Quinazolines - pharmacology
Rats
receptor protein-tyrosine kinase
smooth muscle
stimulatory effects
tetrodotoxin
Tetrodotoxin - pharmacology
Evodia rutaecarpa
cholinergic nervous
evodiamine
stimulatory effects
Ca2
jejunal contractility
Online AccessGet full text
ISSN1478-6419
1478-6427
1478-6427
DOI10.1080/14786419.2014.947485

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Abstract This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca 2+ channel blocker nifedipine or abolished in the Ca 2+ -free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca 2+ -dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.
AbstractList This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5–80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca ²⁺ channel blocker nifedipine or abolished in the Ca ²⁺-free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca ²⁺-dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.
This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca(2+) channel blocker nifedipine or abolished in the Ca(2+)-free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca(2+)-dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca(2+) channel blocker nifedipine or abolished in the Ca(2+)-free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca(2+)-dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.
This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca 2+ channel blocker nifedipine or abolished in the Ca 2+ -free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca 2+ -dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.
This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM) increased normal jejunal contractility and jejunal hypocontractility established under a variety of experimental conditions. Evodiamine-exerted stimulatory effects were blocked by the L-type Ca(2+) channel blocker nifedipine or abolished in the Ca(2+)-free assay condition. The stimulatory effects of evodiamine on jejunal contractility were partially blocked in the presence of neurotoxin tetrodotoxin or endogenous acetylcholine synthesis blocker hemicholinium-3 or muscarinic receptor antagonist atropine, respectively. Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib. Evodiamine increased myosin phosphorylation in jejunal smooth muscle of constipation-prominent rats. These results showed that evodiamine-exerted stimulatory effects on jejunal segments are Ca(2+)-dependent, need the presence of interstitial cell of Cajal, requirement of cholinergic neuron and correlate with increased myosin phosphorylation, implicating the potential value of evodiamine in relieving hypo-motility disorders.
Author Wang, Jing-Yu
Lv, Bo-Chao
Lin, Yuan
Xiong, Yong-Jian
Liu, Fang-Fei
Chen, Da-Peng
Peng, Jin-Yong
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Keywords Evodia rutaecarpa
cholinergic nervous
evodiamine
stimulatory effects
Ca2
jejunal contractility
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Snippet This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM)...
This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5-80.0 μM)...
This study was designed to characterise the effects of evodiamine on intestinal contractility and reveal the correlated mechanisms. Evodiamine (2.5–80.0 μM)...
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SubjectTerms acetylcholine
Animals
antagonists
atropine
calcium
Calcium - metabolism
Calcium Channel Blockers - pharmacology
cholinergic nervous
Evodia rutaecarpa
evodiamine
Gastrointestinal Motility - drug effects
jejunal contractility
jejunum
Jejunum - drug effects
Molecular Structure
Muscle Contraction - drug effects
myosin
Myosins - metabolism
neurons
Nifedipine - pharmacology
Phosphorylation
Quinazolines - pharmacology
Rats
receptor protein-tyrosine kinase
smooth muscle
stimulatory effects
tetrodotoxin
Tetrodotoxin - pharmacology
Title Characteristics of evodiamine-exerted stimulatory effects on rat jejunal contractility
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