Quercetin pretreated umbilical cord mesenchymal stem cells alleviate inflammatory bowel disease via IL-10 /Janus kinase 2/STAT3 signaling

doi:10.4252/wjsc.v17.i9.105896

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World Journal of Stem Cells

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1948-0210

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Stem Cells. Sep 26, 2025; 17(9): 105896
Published online Sep 26, 2025. doi: 10.4252/wjsc.v17.i9.105896

Quercetin pretreated umbilical cord mesenchymal stem cells alleviate inflammatory bowel disease via IL-10 /Janus kinase 2/STAT3 signaling

Meng-Yue Shi, Lian Liu, Fu-Yuan Yang

Meng-Yue Shi, Fu-Yuan Yang, Department of Anesthesiology, The First Affiliated Hospital of Yangtze University, Jingzhou 434020, Hubei Province, China

Meng-Yue Shi, School of Medicine, Yangtze University, Jingzhou 434023, Hubei Province, China

Lian Liu, Department of Pharmacology, Medical School of Yangtze University, Jingzhou 434023, Hubei Province, China

Fu-Yuan Yang, Health Science Center, Yangtze University, Jingzhou 434020, Hubei Province, China

Author contributions: Shi MY, Liu L, and Yang FY contributed to the conception and design, collection and/or assembly of the data, data analyses, and interpretation of the manuscript; Shi MY wrote the manuscript; Yang FY approved the final manuscript.

Supported by the Science and Technology Research Project of Hubei Province, No. 2021CFB210; and Central Guiding Local Science and Technology Development Fund Project (Science and Technology Department of Xizang Autonomous Region), No. XZ202401YD0002C.

Institutional review board statement: The study was reviewed and approved by the Ethics Committee of Health Science Center of Yangtze University, Approval No. CJYXBEC2021-135.

Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Ethics Committee of Health Science Center of Yangtze University (Approval No. CJYXBEC2021-135).

Conflict-of-interest statement: The authors have no conflicts of interest to declare.

ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.

Data sharing statement: The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

Corresponding author: Fu-Yuan Yang, PhD, Department of Anesthesiology, The First Affiliated Hospital of Yangtze University, No. 55 Jianghan North Road, Shashi District, Jingzhou 434020, Hubei Province, China. ivansblue@sina.com

Received: February 10, 2025
Revised: April 7, 2025
Accepted: August 4, 2025
Published online: September 26, 2025
Processing time: 226 Days and 19.6 Hours

Abstract

BACKGROUND

Inflammatory bowel disease (IBD) is a chronic, progressive inflammatory condition of the intestine. Mesenchymal stem cell (MSC) therapy for IBD has made significant progress in recent years. To better exploit the therapeutic potential of MSCs, pretreatment strategies are employed to enhance their therapeutic capabilities. As a compound with diverse pharmacological effects, quercetin (QUR) is applied to pretreat human umbilical cord-derived MSCs (hUCMSCs) in this study, thereby augmenting their immunotherapeutic potential.

AIM

To evaluate the therapeutic efficacy of QUR-pretreated hUCMSCs.

METHODS

We induced colitis in a mouse model using a 2,4,6-trinitrobenzenesulfonic acid solution. Intraperitoneal injection of QUR-pretreated hUCMSCs significantly improved clinical and pathological manifestations of colitis compared to the model group. Interestingly, the therapeutic effect was superior to that of untreated hUCMSCs. Mice exhibited significantly reduced weight loss, diminished infiltration of inflammatory cells observed in hematoxylin and eosin staining, improved Disease Activity Index and Histological Activity Index scores. Furthermore, colonic tissue analysis revealed a significant upregulation of the anti-inflammatory cytokine interleukin 10 (IL-10), accompanied by a downregulation of the pro-inflammatory cytokine IL-6. Further tests also suggested that QUR pretreatment led to inhibition of Janus kinase/signal transducer and activator of transcription (STAT) phosphorylation.

RESULTS

Our study demonstrated that QUR pretreatment of hUCMSCs significantly enhanced their immune-regulatory capacity. This approach effectively mitigated colonic inflammation in a mouse colitis model by modulating the IL-10/Janus kinase/STAT signaling pathway.

CONCLUSION

These findings suggest that QUR pretreatment acts synergistically to augment the inherent anti-inflammatory and immune-regulatory properties of hUCMSCs, resulting in enhanced therapeutic efficacy for IBD treatment.

Keywords: Quercetin; Human umbilical cord-derived mesenchymal stem cells; Inflammatory bowel disease; Interleukin 10; Janus kinase; Signal transducer and activator of transcription; Suppressor of cytokine signaling signal

Core Tip: Quercetin (QUR) pretreatment enhanced the viability of human umbilical cord-derived mesenchymal stem cells (hUCMSCs), which may improve their immune regulatory ability. Intraperitoneal injection of QUR-hUCMSCs effectively alleviated inflammation in 2,4,6-trinitrobenzenesulfonic acid mice, and the therapeutic effect was superior to untreated hUCMSCs. QUR-hUCMSC treatment significantly enhanced interleukin 10 (IL-10) expression in 2,4,6-trinitrobenzenesulfonic acid mice. QUR-hUCMSCs inhibited inflammatory bowel disease inflammation by regulating the IL-10/Janus kinase/signal transducer and activator of transcription signaling pathway.