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ORIGINAL RESEARCH article

Front. Pharmacol.
Sec. Gastrointestinal and Hepatic Pharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1424400
This article is part of the Research Topic The Roles of Pathogens in Gut-Related Diseases and the Strategies for Inhibiting Their Growth View all 9 articles

Emodin Repair Gallbladder Interstitial cells of Cajal Damage in Cholelithiasis

Provisionally accepted
ZHENPENG HUANG ZHENPENG HUANG 1*Hu Qiu Hu Qiu 2
  • 1 Guangxi University of Chinese Medicine, Nanning, China
  • 2 Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China

The final, formatted version of the article will be published soon.

    Background: Hypercholesterolemia induces cholelithiasis and dysfunction of gallbladder motility. Interstitial cells of Cajal (ICCs) contribute to gallbladder motility. Emodin modulates the contractility of the gallbladder muscle; however, the underlying mechanism is unknown.Aim: This study aimed to explore the effects of emodin on gallbladder ICCs with cholelithiasis in a guinea pig model. Methods: Animals were randomly divided into a healthy control group and three study groups. All study groups received a high-cholesterol diet (HCD) for 8 weeks. Subsequently, they were randomly assigned to either the HCD group or one of the emodin treatment groups lasting 4 or 8 weeks. Total cholesterol (TC) and triglyceride (TG) were measured to determine changes in serum lipid levels.Immunohistochemistry was performed to detect the morphology and number of ICCs.TUNEL assays were performed to detect ICC apoptosis. Transmission electron microscopy was employed to observe ICC structure. Western blotting and real-time polymerase chain reaction were used to detect changes in stem cell factor (SCF)/c-kit pathway expression.Results: Serum TC and TG were higher in all study groups. In cases of cholelithiasis, SCF/c-kit pathway was downregulated, the number of gallbladder ICCs were decreased, apoptosis was increased, and the ICCs network structure was damaged. After emodin treatment, SCF/c-kit pathway upregulated, the number of gallbladder ICC increased, apoptosis decreased, and the ICCs network structure recovered.Cholelithiasis downregulates SCF/c-kit pathway and damages gallbladder ICCs. Emodin upregulates SCF/c-kit pathway and increases gallbladder ICCs, contributing to recovery from gallbladder motility disorders.

    Keywords: Interstitial Cells of Cajal, SCF/c-kit pathway, Gallbladder, Cholelithiasis, Emodin

    Received: 28 Apr 2024; Accepted: 27 Aug 2024.

    Copyright: © 2024 HUANG and Qiu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: ZHENPENG HUANG, Guangxi University of Chinese Medicine, Nanning, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.