Evidence map›Paper›PMID 27609334›Full record

ArticleJournal of neuroinflammation2016

Glycyrrhizin protects against focal cerebral ischemia via inhibition of T cell activity and HMGB1-mediated mechanisms.

Xiaoxing Xiong, Lijuan Gu, Yan Wang, Ying Luo, Hongfei Zhang, Jessica Lee, Sheri Krams, Shengmei Zhu, Heng Zhao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

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  19. The Role of Supplementation with Natural Compounds in Post-Stroke Patients.International journal of molecular sciences · 2021
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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 5 institutions in 2 countries.

Xiaoxing XiongDepartment of Anesthesia, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, People's Republic of China.
Lijuan GuDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA.
Yan WangDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA.
Ying LuoDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA.
Hongfei ZhangDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA.
Jessica LeeDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA.
Sheri KramsDepartment of Surgery, Stanford University, Stanford, CA, 94305, USA.
Shengmei ZhuDepartment of Anesthesia, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, People's Republic of China. smzhu20088@163.com.
Heng ZhaoDepartment of Neurosurgery and Stanford Stroke Center, Stanford University, 1201 Welch Rd, Stanford, CA, 94305, USA. hzhao@stanford.edu.ORCID 0000-0003-4180-653X
Stanford University · USWuhan University · CNHangzhou First People's Hospital · CNStanford Health Care · USZhujiang Hospital · CN

Funding

Protective mechanisms of ischemic postconditioningR01NS064136 · NINDS · STANFORD UNIVERSITY · PI STEINBERG, GARY K · 2010 to 2020
$3.1M
NINDS NIH HHS R01 NS064136
6 · The paper itself

Abstract

backgroundGlycyrrhizin (Gly) protects against brain injury induced by stroke. We studied whether Gly achieves its protection by inhibiting T cell activity and high-mobility group box 1 (HMGB1) release in the ischemic brain.

methodsStroke was induced by transient middle cerebral artery occlusion in rats and mice. Gly was injected intraperitoneally before or after stroke. We measured infarction, neuroinflammatory cells, gene expressions of interferon-γ (IFNγ), IL-4, and IL-10 in CD4 T cells, HMGB1 release, and T cell proliferation in cultured splenocytes.

resultsGly treatment reduced infarctions and neuroinflammation characterized by the infiltration of CD68-positive macrophages and myeloperoxidase-positive neutrophils, which corresponds to a reduction in the number of T cells and their subsets, CD4 and CD8 T cells, in the ischemic brain, as measured by flow cytometry. Unlike in wild-type animals, Gly did not offer protection in nude rats and severe combined immunodeficient (SCID) mice who had no T cells, while Gly reduced infarction in both nude rats and SCID mice whose T cells were reconstituted, suggesting that T cells should be the target of Gly. In addition, Gly administration inhibited T cell proliferation stimulated by ConA in in vitro assays and inhibited HMGB1 release from the ischemic brain. Furthermore, Gly attenuated gene expression of IFNγ, but not IL-4 and IL-10 in CD4 T cells. Lastly, HMGB1 promoted T cell proliferation stimulated by ConA, which was inhibited by the addition of Gly.

conclusionsGly blocks infarction by inhibiting IFNγ-mediated T cell activity, which is at least partly modulated by HMGB1 activity.

Indexed as

AnimalsAnti-Inflammatory AgentsBrainBrain InfarctionBrain IschemiaCell ProliferationConcanavalin ACytokinesDisease Models, AnimalGene Expression RegulationGlycyrrhizic AcidHMGB1 ProteinMiceMice, Inbred C57BLMice, SCIDPhosphopyruvate HydrataseAnti-Inflammatory AgentsConcanavalin ACytokinesGlycyrrhizic AcidHMGB1 ProteinPhosphopyruvate HydrataseCerebral ischemiaGlycyrrhizinHMGB1T cells

Identifiers

PMID27609334
PMCPMC5016958
OpenAlexW2516419500

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.