Evidence map›Paper›PMID 25762107›Full record

ArticleScientific reports2015

Kirenol attenuates experimental autoimmune encephalomyelitis by inhibiting differentiation of Th1 and th17 cells and inducing apoptosis of effector T cells.

Juan Xiao, Rongbing Yang, Lin Yang, Xiaohang Fan, Wenwei Liu, Wenbin Deng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Juan Xiao1] Medical College, Hubei University of Arts and Science, Xiangyang, Hubei, China [2] Department of Biological Treatment, Handan Central Hospital, Handan, Hebei, China [3] Department of Biochemistry and Molecular Medicine, School of Medicine, University of California, Davis, CA, USA.
Rongbing YangDepartment of Biological Treatment, Handan Central Hospital, Handan, Hebei, China.
Lin YangMedical College, Hubei University of Arts and Science, Xiangyang, Hubei, China.
Xiaohang FanMedical College, Hubei University of Arts and Science, Xiangyang, Hubei, China.
Wenwei LiuMedical College, Hubei University of Arts and Science, Xiangyang, Hubei, China.
Wenbin Deng1] Medical College, Hubei University of Arts and Science, Xiangyang, Hubei, China [2] Department of Biochemistry and Molecular Medicine, School of Medicine, University of California, Davis, CA, USA.
Hubei University of Arts and Science · CNHandan College · CN

Funding

Oligodendrocytes, Glutamate Receptors, and Lead NeurotoxicityR01ES015988 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DENG, WENBIN · 2007 to 2011
$2.0M
Glutamate Receptors in Hypoxic-ischemic Injury to Developing OligodendrocytesR01NS059043 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DENG, WENBIN · 2008 to 2012
$1.4M
NIEHS NIH HHS R01 ES015988NINDS NIH HHS R01 NS059043
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), is characterized by CNS demyelination mediated by autoreactive T cells. Kirenol, a biologically active substance isolated from Herba Siegesbeckiae, has potent anti-inflammatory activities. Here we investigated effects of kirenol on EAE. Kirenol treatment markedly delayed onset of disease and reduced clinical scores in EAE mice. Kirenol treatment reduced expression of IFN-γ and IL-17A in the serum and proportion of Th1 and Th17 cells in draining lymph nodes. Priming of lymphocytes was reduced and apoptosis of MOG-activated CD4+ T cells was increased in kirenol treated EAE mice. Kirenol treatment of healthy animals did not affect the lymphocytes in these non-immunized mice. Further in vitro studies showed that kirenol inhibited viability of MOG-specific lymphocytes and induced apoptosis of MOG-specific CD4+ T cells in a dose- and time-dependent manner. Kirenol treatment upregulated Bax,downregulated Bcl-2,and increased activation of caspase-3 and release of cytochrome c, indicating that a mitochondrial pathway was involved in kirenol induced apoptosis. Moreover, pretreatment with either a pan-caspase inhibitor z-VAD-fmk or a more specific caspase 3 inhibitor Ac-DEVD-CHO in lymphocytes reduced kirenol induced apoptosis. Our findings implicate kirenol as a useful agent for the treatment of MS.

Indexed as

AnimalsApoptosisCell DifferentiationCytokinesDiterpenesEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunologic MemoryMiceMitochondriaMyelin-Oligodendrocyte GlycoproteinSignal TransductionT-Cell Antigen Receptor SpecificityTh17 CellsTh1 CellsT-Lymphocyte SubsetsCytokinesDiterpeneskirenolMyelin-Oligodendrocyte Glycoprotein

Identifiers

PMID25762107
PMCPMC4356981
OpenAlexW1971475979

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.