Evidence map›Paper›PMID 33788130›Full record

ArticleInflammation2021

9,10-Anhydrodehydroartemisinin Attenuates Experimental Autoimmune Encephalomyelitis by Inhibiting Th1 and Th17 Cell Differentiation.

Jie Lv, Wei Zhuang, Yan Zhang, Ling Xie, Zhenglong Xiang, Qingjie Zhao, Xiangrui Jiang, Jingshan Shen, Changsheng Du

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Journal of oral microbiology · 2026
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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

9 authors at 3 institutions in 1 country.

Jie LvPutuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Wei ZhuangPutuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Yan ZhangXinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, 40-1 Beijing Road, Urumqi, 830011, Xinjiang, China.
Ling XiePutuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Zhenglong XiangPutuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.
Qingjie ZhaoCAS Key Laboratory for Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai, 201203, China.
Xiangrui JiangUniversity of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing, 100049, China. jiangxiangrui@simm.ac.cn.
Jingshan ShenUniversity of Chinese Academy of Sciences, No.19A Yuquan Road, Beijing, 100049, China.
Changsheng DuPutuo People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China. duchangsheng@tongji.edu.cn.ORCID http://orcid.org/0000-0002-7922-9785
Tongji University · CNChinese Academy of Sciences · CNShanghai Institute of Materia Medica · CN

Funding

the National Natural Science Foundation of China 31871404the National Natural Science Foundation of China 31900658the National Natural Science Foundation of China 32070768
6 · The paper itself

Abstract

Human inflammatory disease, multiple sclerosis (MS), is a demyelinating disease of central nervous system (CNS). The experimental autoimmune encephalomyelitis (EAE) is the most commonly used as experimental model because of its key pathological features' approximation of MS. The interaction between complex elements in immune system and in the CNS determines the MS pathogenesis. However, there is no cure for MS and the treatment for MS still encounters great challenges. Thus, finding a more effective disease-modifying treatment is imminent. In the present study, we investigated whether 9,10-Anhydrodehydroartemisin (ADART), a compound derived from artemisinin, could decrease demyelination in EAE and the underlying mechanisms. In established EAE mice, 100 mg/kg 9,10-Anhydrodehydroartemisinin (ADART) effectively reduced CNS and peripheral immune system infiltration inflammatory cells including CD4

Indexed as

Amino Acid SequenceAnimalsArtemisininsCell DifferentiationDose-Response Relationship, DrugEncephalomyelitis, Autoimmune, ExperimentalMaleMiceMice, Inbred C57BLTh17 CellsTh1 CellsanhydrodihydroartemisininArtemisinins9, 10-Anhydrodehydroartemisininartemisininexperimental autoimmune encephalomyelitismultiple sclerosisTh1/Th17

Identifiers

PMID33788130
OpenAlexW3143553821

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.