Xuesanqi ameliorates DSS‑induced colitis in mice by mediating gut microbiota dysbiosis and modulating MAPK/ERK/JNK pathway

Qiyuan Su; Qian Hu; Songtao Wu; Suqin Wang; Hanwen Su; Zhengjun Zhang; Chengxiu Ling

Xuesanqi ameliorates DSS‑induced colitis in mice by mediating gut microbiota dysbiosis and modulating MAPK/ERK/JNK pathway

Qiyuan Su
, Qian Hu
, Songtao Wu
, Suqin Wang
, Hanwen Su^*
, Zhengjun Zhang
, Chengxiu Ling^*

^*Corresponding author for this work

Xi'an Jiaotong‐Liverpool University
Wuhan Children’s Hospital, Tongji Medical College, Huazhong University of Science and Technology,
Faculty of Pharmacy, Hubei University of Chinese Medicine
School of Pharmaceutical Sciences, South-Central Minzu University
Department of Clinical Laboratory, Renmin Hospital of Wuhan University
Department of Statistics, University of Wisconsin-Madison,
School of Economics and Management, and MOE Social Science Laboratory of Digital Economic Forecasts and Policy Simulation, University of Chinese Academy of Sciences, Center for Forecasting Sciences, Chinese Academy of Sciences

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Abstract

This study aimed to evaluate the therapeutic properties of the traditional Chinese medicine Xuesanqi (XSQ,
from the rhizome of Polygonum amplexicaule D. Don) in treating ulcerative colitis. We hypothesized that its many
active components can alleviate symptoms of colitis by regulating the gut microbiota, its metabolites, and various
signaling pathways. To test our hypotheses, we designed a DSS- induced colitis model in C57BL/6 male mice.
Apparent metrics were evaluated in each group of mice and performed histological analysis of relevant tissues.
The gut microbial composition was analyzed by 16S rRNA sequencing of bacteria. Simultaneously, the SCFAs content
was detected by gas chromatography, inflammatory factor secretion was evaluated by ELISA or western-blot,
the expression of tight junction protein and key proteins of the MAPK signaling pathway were analyzed by westernblot.
Our result showed that the treatment with XSQ alleviated significant various symptoms such as weight loss,
blood in stool, and shortening of colon. In addition, XSQ treatment restored the dysregulated gut microbiota in colitis
mice, increased short chain fatty acids (SCFAs) and normalized the MAPK/ERK/JNK signaling pathways, promoted
expression of tight junction protein Occludin, Claudin-1, and E-cadherin proteins. Furthermore, we also observed
a dose-dependent pattern in these treatment responses. These findings demonstrated the active components of XSQ
is a promising new treatment platform for ulcerative colitis.

Original language	English
Journal	Natural Products and Bioprospecting
Publication status	Published - Nov 2024

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@article{05d49ca92b604022880878fe55750356,

title = "Xuesanqi ameliorates DSS‑induced colitis in mice by mediating gut microbiota dysbiosis and modulating MAPK/ERK/JNK pathway",

abstract = "This study aimed to evaluate the therapeutic properties of the traditional Chinese medicine Xuesanqi (XSQ, from the rhizome of Polygonum amplexicaule D. Don) in treating ulcerative colitis. We hypothesized that its many active components can alleviate symptoms of colitis by regulating the gut microbiota, its metabolites, and various signaling pathways. To test our hypotheses, we designed a DSS- induced colitis model in C57BL/6 male mice. Apparent metrics were evaluated in each group of mice and performed histological analysis of relevant tissues. The gut microbial composition was analyzed by 16S rRNA sequencing of bacteria. Simultaneously, the SCFAs content was detected by gas chromatography, inflammatory factor secretion was evaluated by ELISA or western-blot, the expression of tight junction protein and key proteins of the MAPK signaling pathway were analyzed by westernblot. Our result showed that the treatment with XSQ alleviated significant various symptoms such as weight loss, blood in stool, and shortening of colon. In addition, XSQ treatment restored the dysregulated gut microbiota in colitis mice, increased short chain fatty acids (SCFAs) and normalized the MAPK/ERK/JNK signaling pathways, promoted expression of tight junction protein Occludin, Claudin-1, and E-cadherin proteins. Furthermore, we also observed a dose-dependent pattern in these treatment responses. These findings demonstrated the active components of XSQ is a promising new treatment platform for ulcerative colitis.",

author = "Qiyuan Su and Qian Hu and Songtao Wu and Suqin Wang and Hanwen Su and Zhengjun Zhang and Chengxiu Ling",

year = "2024",

month = nov,

language = "English",

journal = "Natural Products and Bioprospecting",

}

TY - JOUR

T1 - Xuesanqi ameliorates DSS‑induced colitis in mice by mediating gut microbiota dysbiosis and modulating MAPK/ERK/JNK pathway

AU - Su, Qiyuan

AU - Hu, Qian

AU - Wu, Songtao

AU - Wang, Suqin

AU - Su, Hanwen

AU - Zhang, Zhengjun

AU - Ling, Chengxiu

PY - 2024/11

Y1 - 2024/11

N2 - This study aimed to evaluate the therapeutic properties of the traditional Chinese medicine Xuesanqi (XSQ, from the rhizome of Polygonum amplexicaule D. Don) in treating ulcerative colitis. We hypothesized that its many active components can alleviate symptoms of colitis by regulating the gut microbiota, its metabolites, and various signaling pathways. To test our hypotheses, we designed a DSS- induced colitis model in C57BL/6 male mice. Apparent metrics were evaluated in each group of mice and performed histological analysis of relevant tissues. The gut microbial composition was analyzed by 16S rRNA sequencing of bacteria. Simultaneously, the SCFAs content was detected by gas chromatography, inflammatory factor secretion was evaluated by ELISA or western-blot, the expression of tight junction protein and key proteins of the MAPK signaling pathway were analyzed by westernblot. Our result showed that the treatment with XSQ alleviated significant various symptoms such as weight loss, blood in stool, and shortening of colon. In addition, XSQ treatment restored the dysregulated gut microbiota in colitis mice, increased short chain fatty acids (SCFAs) and normalized the MAPK/ERK/JNK signaling pathways, promoted expression of tight junction protein Occludin, Claudin-1, and E-cadherin proteins. Furthermore, we also observed a dose-dependent pattern in these treatment responses. These findings demonstrated the active components of XSQ is a promising new treatment platform for ulcerative colitis.

AB - This study aimed to evaluate the therapeutic properties of the traditional Chinese medicine Xuesanqi (XSQ, from the rhizome of Polygonum amplexicaule D. Don) in treating ulcerative colitis. We hypothesized that its many active components can alleviate symptoms of colitis by regulating the gut microbiota, its metabolites, and various signaling pathways. To test our hypotheses, we designed a DSS- induced colitis model in C57BL/6 male mice. Apparent metrics were evaluated in each group of mice and performed histological analysis of relevant tissues. The gut microbial composition was analyzed by 16S rRNA sequencing of bacteria. Simultaneously, the SCFAs content was detected by gas chromatography, inflammatory factor secretion was evaluated by ELISA or western-blot, the expression of tight junction protein and key proteins of the MAPK signaling pathway were analyzed by westernblot. Our result showed that the treatment with XSQ alleviated significant various symptoms such as weight loss, blood in stool, and shortening of colon. In addition, XSQ treatment restored the dysregulated gut microbiota in colitis mice, increased short chain fatty acids (SCFAs) and normalized the MAPK/ERK/JNK signaling pathways, promoted expression of tight junction protein Occludin, Claudin-1, and E-cadherin proteins. Furthermore, we also observed a dose-dependent pattern in these treatment responses. These findings demonstrated the active components of XSQ is a promising new treatment platform for ulcerative colitis.

M3 - Article

JO - Natural Products and Bioprospecting

JF - Natural Products and Bioprospecting

ER -

Xuesanqi ameliorates DSS‑induced colitis in mice by mediating gut microbiota dysbiosis and modulating MAPK/ERK/JNK pathway

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