Evidence map›Paper›PMID 33179078›Full record

ArticleMolecular medicine reports2021

Curcumin ameliorates DSS‑induced colitis in mice by regulating the Treg/Th17 signaling pathway.

Cheng Wei, Jian-Yao Wang, Feng Xiong, Ben-Hua Wu, Ming-Han Luo, Zhi-Chao Yu, Ting-Ting Liu, De-Feng Li, Qi Tang, Ying-Xue Li and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 12% of its field
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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

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  8. Antioxidants (Basel, Switzerland) · 2025
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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

15 authors at 3 institutions in 1 country.

Cheng Wei *Department of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Jian-Yao Wang *Department of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong 518026, P.R. China.
Feng Xiong *Department of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Ben-Hua Wu *Department of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Ming-Han LuoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Zhi-Chao YuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Ting-Ting LiuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
De-Feng LiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Qi TangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Ying-Xue LiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Ding-Guo ZhangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Zheng-Lei XuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Hong-Tao JinDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Li-Sheng WangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Jun YaoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.
Jinan University · CNShenzhen Second People's Hospital · CNShenzhen Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin has a therapeutic effect on ulcerative colitis, but the underlying mechanism has yet to be elucidated. The aim of the present study was to clarify the possible mechanisms. Dextran sulfate sodium‑induced colitis mice were treated with curcumin via gavage for 7 days. The effects of curcumin on disease activity index (DAI) and pathological changes of colonic tissue in mice were determined. Interleukin (IL)‑6, IL‑10, IL‑17 and IL‑23 expression levels were measured by ELISA. Flow cytometry was used to detect the ratio of mouse spleen regulatory T cells (Treg)/Th17 cells, and western blotting was used to measure the nuclear protein hypoxia inducible factor (HIF)‑1α level. The results demonstrated that curcumin can significantly reduce DAI and spleen index scores and improve mucosal inflammation. Curcumin could also regulate the re‑equilibration of Treg/Th17. IL‑10 level in the colon was significantly increased, while inflammatory cytokines IL‑6, IL‑17 and IL‑23 were significantly reduced following curcumin treatment. No significant difference in HIF‑1α was observed between the colitis and the curcumin group. It was concluded that oral administration of curcumin can effectively treat experimental colitis by regulating the re‑equilibration of Treg/Th17 and that the regulatory mechanism may be closely related to the IL‑23/Th17 pathway. The results of the present study provided molecular insight into the mechanism by which curcumin treats ulcerative colitis.

Indexed as

Administration, OralAnimalsColitis, UlcerativeCurcuminCytokinesDextran SulfateDisease Models, AnimalGene Expression RegulationMaleMiceMice, Inbred BALB CSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryTreatment OutcomeCurcuminCytokinesDextran Sulfatecurcumininflammatory bowel diseaseThelper 17 cellsT regulatory cells

Identifiers

PMID33179078
PMCPMC7684861
OpenAlexW3102382822

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.