Effect of emodin on small intestinal peristalsis of mice and relevant mechanism

Hong-Quan Zhang1, Cheng-Hua Zhou, Yu-Qing Wu

  • 1Medical and Pharmacological Institute, Yangzhou University, Yangzhou 225001, Jiangsu Province, China. lixin2001@sohu.com

Abstract

Insights

Emodin enhances small intestinal peristalsis in mice by increasing motilin and decreasing somatostatin. It also inhibits Na+-K+-ATPase activity, impacting nutrient transport.

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Physiology

Background:

  • Small intestinal peristalsis is crucial for digestion and nutrient absorption.
  • Motilin and somatostatin are key hormones regulating gastrointestinal motility.
  • Emodin, a natural compound, has shown various biological activities.

Purpose of the Study:

  • To investigate the effects of emodin on mouse small intestinal peristalsis.
  • To elucidate the underlying mechanisms of emodin's action on gastrointestinal motility.

Main Methods:

  • Charcoal powder propulsion test to assess intestinal transit.
  • Radioimmunoassay to quantify motilin and somatostatin levels.
  • Measurement of electrical potential difference (PD) and Na+-K+-ATPase activity.

Main Results:

  • Emodin significantly improved small intestinal peristalsis in a dose-dependent manner.
  • Emodin increased motilin and decreased somatostatin concentrations.
  • Emodin inhibited Na+-K+-ATPase activity and affected glucose-dependent PD.

Conclusions:

  • Emodin enhances small intestinal peristalsis by modulating motilin and somatostatin.
  • Inhibition of Na+-K+-ATPase activity is a potential mechanism for emodin's effect.
  • Emodin shows promise as a therapeutic agent for motility disorders.

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