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已发表论文
二氢杨梅素通过抑制肠道菌群失调引起的 NLRP3 炎性小体活化改善溃疡性结肠炎
Authors Chen J, Ding S, Yang H, Dai Y, Zhang Z, Zhu T, Cao L, Hu B, Liu H
Received 7 June 2025
Accepted for publication 21 November 2025
Published 13 December 2025 Volume 2025:18 Pages 17401—17420
DOI https://doi.org/10.2147/JIR.S545159
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Nadia Andrea Andreani
Jun Chen,1,2,* Shengchen Ding,1,2,* Huabing Yang,1,2 Yi Dai,3 Zhigang Zhang,1,2 Tianxiang Zhu,1,2 Lu Cao,1,2 Baifei Hu,1,2 Hongtao Liu1,2,4
1College of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan, 430065, People’s Republic of China; 2Hubei Shizhen Laboratory, Wuhan, 430061, People’s Republic of China; 3Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 430022, People’s Republic of China; 4Key Laboratory of Chinese Medicinal Resource and Chinese Herbal Compound of the Ministry of Education, Wuhan, 430065, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Baifei Hu, Email baifeihu3452@hbucm.edu.cn Hongtao Liu, Email hongtaoliu@hbucm.edu.cn
Purpose: Dihydromyricetin (DMY) is known for its wide range of pharmacological effects and has been approved as a dietary supplement. This study aimed to investigate the therapeutic effects of DMY on dextran sulfate sodium (DSS)-induced disruption of intestinal homeostasis in mice and to explore the underlying molecular mechanisms.
Methods: To establish a model of colitis, mice were treated with a 3% DSS solution, followed by gavage administration of DMY for therapeutic intervention. Techniques such as histomorphology, RT-qPCR, 16S rRNA sequencing, and Western blot analysis were used.
Results: DMY alleviated several physiological symptoms in colitis mice, including a reduction in the disease activity index (DAI) and spleen index, as well as decreases in the numbers of white blood cells, lymphocytes, and monocytes. Additionally, DMY helped repair the intestinal mucosal barrier function, reshaped the composition of gut microbiota, and regulated intestinal immune responses. These effects collectively contributed to the partial restoration of intestinal homeostasis in colitis mice. Furthermore, experiments with NLRP3−/− mice and pseudo-germ-free mice confirmed that DMY exerts its anti-colitis effects through the gut microbiota-NLRP3 inflammasome axis.
Conclusion: DMY helps regulate intestinal homeostasis in colitis mice by suppressing the NLRP3 inflammasome via the gut microbiota. Our study provides new evidence supporting DMY as a potential therapeutic agent for colitis.
Keywords: dihydromyricetin, ulcerative colitis, NLRP3 inflammasome, gut microbiota, intestinal homeostasis
1College of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan, 430065, People’s Republic of China; 2Hubei Shizhen Laboratory, Wuhan, 430061, People’s Republic of China; 3Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 430022, People’s Republic of China; 4Key Laboratory of Chinese Medicinal Resource and Chinese Herbal Compound of the Ministry of Education, Wuhan, 430065, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Baifei Hu, Email baifeihu3452@hbucm.edu.cn Hongtao Liu, Email hongtaoliu@hbucm.edu.cn
Purpose: Dihydromyricetin (DMY) is known for its wide range of pharmacological effects and has been approved as a dietary supplement. This study aimed to investigate the therapeutic effects of DMY on dextran sulfate sodium (DSS)-induced disruption of intestinal homeostasis in mice and to explore the underlying molecular mechanisms.
Methods: To establish a model of colitis, mice were treated with a 3% DSS solution, followed by gavage administration of DMY for therapeutic intervention. Techniques such as histomorphology, RT-qPCR, 16S rRNA sequencing, and Western blot analysis were used.
Results: DMY alleviated several physiological symptoms in colitis mice, including a reduction in the disease activity index (DAI) and spleen index, as well as decreases in the numbers of white blood cells, lymphocytes, and monocytes. Additionally, DMY helped repair the intestinal mucosal barrier function, reshaped the composition of gut microbiota, and regulated intestinal immune responses. These effects collectively contributed to the partial restoration of intestinal homeostasis in colitis mice. Furthermore, experiments with NLRP3−/− mice and pseudo-germ-free mice confirmed that DMY exerts its anti-colitis effects through the gut microbiota-NLRP3 inflammasome axis.
Conclusion: DMY helps regulate intestinal homeostasis in colitis mice by suppressing the NLRP3 inflammasome via the gut microbiota. Our study provides new evidence supporting DMY as a potential therapeutic agent for colitis.
Keywords: dihydromyricetin, ulcerative colitis, NLRP3 inflammasome, gut microbiota, intestinal homeostasis