Evidence map›Paper›PMID 42540411›Full record

ArticlePrecision clinical medicine2026

Hudi enteric-coated capsule and its active constituent polydatin suppress Th1/Th17-mediated intestinal inflammation by modulating the KEAP1-NFE2L2 signaling pathway.

Xiaohan Wu, Lei Shi, Lei Zhu, Tangyou Mao, Zhibin Wang, Fushun Kou, Xiao Han, Han Gao, Xiaohua Chen, Xianxin Li and 3 more

Abstract read
In one paragraph

Article in Precision clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Xiaohan WuXinxiang Key Laboratory of Precision Diagnosis and Treatment for Inflammatory Bowel Disease, Henan Key Laboratory of the Prevention and Treatment of Gastrointestinal Cancer, Department of Gastroenterology, the First Affiliated Hospital of Henan Medical University, Xinxiang 453100, China.
Lei ShiDepartment of Gastroenterology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China.
Lei ZhuDepartment of Gastroenterology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Tangyou MaoDepartment of Gastroenterology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China.
Zhibin WangDepartment of Gastroenterology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China.
Fushun KouThe First School of Clinical Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China.
Xiao HanInnovative Technology Center, The Ministry of Science and Technology (MOST), Beijing 100862, China.
Han GaoCenter for Inflammatory Bowel Disease Research and Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Xiaohua ChenDepartment of Gastroenterology, Luohe Central Hospital, Luohe 462000, China.
Xianxin LiSchool of Pharmacy, Hubei University of Chinese Medicine, Wuhan 430065, China.
Tingmin ChangXinxiang Key Laboratory of Precision Diagnosis and Treatment for Inflammatory Bowel Disease, Henan Key Laboratory of the Prevention and Treatment of Gastrointestinal Cancer, Department of Gastroenterology, the First Affiliated Hospital of Henan Medical University, Xinxiang 453100, China.
Junxiang LiDepartment of Gastroenterology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China.
Zhanju LiuCenter for Inflammatory Bowel Disease Research and Department of Gastroenterology, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou 215100, China.ORCID https://orcid.org/0000-0002-0326-543X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the anti-inflammatory mechanisms of Hudi enteric-coated capsule (HDEC) and its major bioactive constituent, polydatin, in ulcerative colitis (UC). Methods: Mouse models of colitis were established by transplantation adoptive transfer of CD45RB Results: Treatment with HDEC and polydatin significantly ameliorated murine colitis and mucosal damage. Mechanistically, polydatin directly binds to KEAP1 to promote NFE2L2 nuclear translocation. This NFE2L2 activation reduces intracellular oxidative stress, thereby inhibiting pathogenic Th1/Th17 differentiation and enhancing Treg generation. Importantly, these effects were consistently validated in human CD4 Conclusion: HDEC and polydatin alleviate UC by targeting the KEAP1-NFE2L2 axis to reduce oxidative stress, thereby restoring the Th1/Th17/Treg balance. This highlights polydatin as a promising KEAP1-targeting agent with strong translational potential.

Indexed as

herbsHudi enteric-coated capsule (HDEC)mucosal immunologypolydatinT cell differentiationulcerative colitis

Identifiers

PMID42540411
PMCPMC13425643

What Socratic holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.