Skip to main content

CORRECTION article

Front. Pharmacol.
Sec. Ethnopharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1516840

Corrigendum: Sini San regulates intestinal flora and short-chain fatty acids to ameliorate hepatocyte apoptosis and relieve CCl4induced liver fibrosis in mice

Provisionally accepted
Qiong Wu Qiong Wu 1Fangsi Zhu Fangsi Zhu 1Yu Yao Yu Yao 1Luyun Chen Luyun Chen 1Yijie Ding Yijie Ding 1Yong Su Yong Su 2*Chaoliang Ge Chaoliang Ge 1*
  • 1 Anhui Medical University, Hefei, China
  • 2 First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China

This article is a correction to:

  1. Sini san regulates intestinal flora and short-chain fatty acids to ameliorate hepatocyte apoptosis and relieve CCl4-induced liver fibrosis in mice

    1. Read original article

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

    Introduction: Si-Ni-San (SNS), a traditional Chinese medicine, is effective in treating liver fibrosis with an unclear mechanism. Although disturbance of intestinal flora and the subsequent secretion of short-chain fatty acids (SCFAs) is suggested to be involved in the progression of liver fibrosis, whether SNS produces the anti-fibrosis effect through the regulation of intestinal flora and SCFAs remains unclear. Methods: In the current study, carbon tetrachloride (CCl4)-treated mice were dosed with SNS to examine the anti-fibrotic effects and the involved mechanism. Biochemical parameters, histological staining, and analyses of fibrotic gene expression were used to evaluate the anti-fibrotic effect of SNS, while intestinal flora and SCFA content were determined by 16S rRNA and LC–MS to evaluate the mechanism. Results: In vivo results showed that SNS improved liver function, reduced hepatocyte apoptosis and FFAR2/3 expression, and restored intestinal dysbiosis and reduced PA, BA, and IsA levels. In vitro experiments showed that PA, BA, and IsA exacerbated TNF-α-induced HepG2 apoptosis. Notably, the protective effects of SNS were compromised in pseudo-sterile mice. Discussion: In conclusion, our experimental results suggest that the disturbance in intestinal flora results in elevated SCFA levels, which further exacerbates hepatocyte apoptosis in liver fibrosis, while SNS suppresses CCl4-induced liver fibrosis at least partially by reinstating intestinal flora homeostasis and reducing SCFA levels.

    Keywords: Sini San, intestinal flora, short-chain fatty acids, Hepatocyte apoptosis, liver fibrosis, pseudo germ-free mice

    Received: 25 Oct 2024; Accepted: 28 Oct 2024.

    Copyright: © 2024 Wu, Zhu, Yao, Chen, Ding, Su and Ge. 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:
    Yong Su, First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui Province, China
    Chaoliang Ge, Anhui Medical University, Hefei, 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.