Evidence map›Paper›PMID 26440666›Full record

ArticleMolecular neurobiology2016

Arctigenin Suppress Th17 Cells and Ameliorates Experimental Autoimmune Encephalomyelitis Through AMPK and PPAR-γ/ROR-γt Signaling.

Wen Li, Zhihui Zhang, Kai Zhang, Zhenyi Xue, Yan Li, Zimu Zhang, Lijuan Zhang, Chao Gu, Qi Zhang, Junwei Hao and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

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  10. Phytochemicals as Immunomodulatory Agents in Melanoma.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Article
  15. Article
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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

14 authors at 3 institutions in 1 country.

Wen LiLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Zhihui ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Kai ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Zhenyi XueLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Yan LiLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Zimu ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Lijuan ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Chao GuLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Qi ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Junwei HaoDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yurong DaLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Zhi YaoLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China.
Ying KongDepartment of Biochemistry and Molecular, Dalian Medical University, Dalian, 116044, China. yingkong@dmu.edu.cn.
Rongxin ZhangLaboratory of Immunology and Inflammation, Department of Immunology and Research Center of Basic Medical Sciences, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Immune Microenvironments and Diseases of Educational Ministry, Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Medical University, Tianjin, 300070, China. rongxinz@yahoo.com.
Tianjin Medical University · CNDalian Medical University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arctigenin is a herb compound extract from Arctium lappa and is reported to exhibit pharmacological properties, including neuronal protection and antidiabetic, antitumor, and antioxidant properties. However, the effects of arctigenin on autoimmune inflammatory diseases of the CNS, multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis (EAE) are still unclear. In this study, we demonstrated that arctigenin-treated mice are resistant to EAE; the clinical scores of arctigenin-treated mice are significantly reduced. Histochemical assays of spinal cord sections also showed that arctigenin reduces inflammation and demyelination in mice with EAE. Furthermore, the Th1 and Th17 cells in peripheral immune organs are inhibited by arctigenin in vivo. In addition, the Th1 cytokine IFN-γ and transcription factor T-bet, as well as the Th17 cytokines IL-17A, IL-17F, and transcription factor ROR-γt are significantly suppressed upon arctigenin treatment in vitro and in vivo. Interestedly, Th17 cells are obviously inhibited in CNS of mice with EAE, while Th1 cells do not significantly change. Besides, arctigenin significantly restrains the differentiation of Th17 cells. We further demonstrate that arctigenin activates AMPK and inhibits phosphorylated p38, in addition, upregulates PPAR-γ, and finally suppresses ROR-γt. These findings suggest that arctigenin may have anti-inflammatory and immunosuppressive properties via inhibiting Th17 cells, indicating that it could be a potential therapeutic drug for multiple sclerosis or other autoimmune inflammatory diseases.

Indexed as

Signal TransductionAdenylate KinaseAnimalsCell DifferentiationCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleFuransGene Expression RegulationLignansLymphoid TissueMice, Inbred C57BLModels, BiologicalNuclear Receptor Subfamily 1, Group F, Member 3p38 Mitogen-Activated Protein KinasesPPAR gammaAdenylate KinasearctigeninCytokinesFuransLignansNuclear Receptor Subfamily 1, Group F, Member 3p38 Mitogen-Activated Protein KinasesPPAR gammaRNA, MessengerAMPKArctigeninExperimental autoimmune encephalomyelitisPPAR-γTh17 cells

Identifiers

PMID26440666
OpenAlexW1840711934

What OpenQuestion holds

Textmetadata
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.