Evidence map›Paper›PMID 31927682›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2020

Calycosin Preserves BDNF/TrkB Signaling and Reduces Post-Stroke Neurological Injury after Cerebral Ischemia by Reducing Accumulation of Hypertrophic and TNF-α-Containing Microglia in Rats.

Chien-Chin Hsu, Ting-Wei Kuo, Wen-Pin Liu, Ching-Ping Chang, Hung-Jung Lin

Abstract read
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In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Herbal medicines for SOD1Frontiers in immunology · 2024
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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

5 authors at 2 institutions in 1 country.

Chien-Chin HsuDepartment of Emergency Medicine, Chi Mei Medical Center, No. 901, Zhonghua Rd., Yongkang District, Tainan City, 710, Taiwan.
Ting-Wei KuoDepartment of Biotechnology and Food Technology, Southern Taiwan University of Science and Technology, Tainan, 710, Taiwan.
Wen-Pin LiuDepartment of Medical Research, Chi Mei Medical Center, No. 901, Zhonghua Rd., Yongkang District, Tainan City, 710, Taiwan.
Ching-Ping ChangDepartment of Medical Research, Chi Mei Medical Center, No. 901, Zhonghua Rd., Yongkang District, Tainan City, 710, Taiwan. jessica.cpchang@gmail.com.ORCID 0000-0003-0890-9414
Hung-Jung LinDepartment of Emergency Medicine, Chi Mei Medical Center, No. 901, Zhonghua Rd., Yongkang District, Tainan City, 710, Taiwan. 790001@mail.chimei.org.tw.
Chi Mei Medical Center · TWSouthern Taiwan University of Science and Technology · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both brain-derived neurotrophic factor (BDNF) and microglia activation are involved in the pathogenesis of ischemic stroke. Herein, we attempt to ascertain whether Calycosin, an isoflavonoid, protects against ischemic stroke by modulating the endogenous production of BDNF and/or the microglia activation. This study was a prospective, randomized, blinded and placebo-controlled preclinical experiment. Sprague-Dawley adult rats, subjected to transient focal cerebral ischemia by middle cerebral artery occlusion (MCAO), were treated randomly with 0 (corn oil and/or saline as placebo), 30 mg/kg of Calycosin and/or 1 mg/kg of a tropomyosin-related kinase B (TrkB) receptor antagonist (ANA12) at 1 h after reperfusion and once daily for a total of 7 consecutive days. BDNF and its functional receptor, full-length TrkB (TrkB-FL) levels, the percentage of hypertrophic microglia, tumor necrosis factor-α (TNF-α)-containing microglia, and degenerative and apoptotic neurons in ischemic brain regions were determined 7 days after cerebral ischemia. A battery of functional sensorimotor test was performed over 7 days. Post-stroke Calycosin therapy increased the cerebral expression of BDNF/TrkB, ameliorated the neurological injury and switched the microglia from the activated amoeboid state to the resting ramified state in ischemic stroke rats. However, the beneficial effects of BDNF/ TrkB-mediated Calycosin could be reversed by ANA12. Our data indicate that BDNF/TrkB-mediated Calycosin ameliorates rat ischemic stroke injury by switching the microglia from the activated amoeboid state to the resting ramified state. Graphical abstract.

Indexed as

AnimalsBrainBrain-Derived Neurotrophic FactorBrain IschemiaDrugs, Chinese HerbalIsoflavonesMaleMicrogliaRatsRats, Sprague-DawleyReceptor, trkBSignal TransductionStrokeTumor Necrosis Factor-alpha7,3'-dihydroxy-4'-methoxyisoflavoneBdnf protein, ratBrain-Derived Neurotrophic FactorDrugs, Chinese HerbalIsoflavonesNtrk2 protein, ratReceptor, trkBTumor Necrosis Factor-alphaBrain-derived neurotrophic factorCalycosinMicrogliaNeuronal deathStroke

Identifiers

PMID31927682
OpenAlexW2999362366

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.