Evidence map›Paper›PMID 35649147›Full record

ArticleJournal of food and drug analysis2021

Medicarpin isolated from Radix Hedysari ameliorates brain injury in a murine model of cerebral ischemia.

Chang-Ming Chern, Chung-Kuang Lu, Kuo-Tong Liou, Yea-Hwey Wang, Keng-Chang Tsai, Chia-Lin Chang, Chia-Che Chang, Yuh-Chiang Shen

Open access · hybridAbstract read
In one paragraph

Article in Journal of food and drug analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Enhanced Inhibition ofInternational journal of molecular sciences · 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

8 authors at 6 institutions in 1 country.

Chang-Ming ChernTaipei Municipal Gan-Dau Hospital, Taipei City, Taiwan.
Chung-Kuang LuNational Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei City, Taiwan.
Kuo-Tong LiouNational Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei City, Taiwan.
Yea-Hwey WangNational Taipei University of Nursing and Health Sciences, Taipei City, Taiwan.
Keng-Chang TsaiNational Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei City, Taiwan.
Chia-Lin ChangResearch Institute of Biotechnology, HungKuang University, Taichung City, Taiwan.
Chia-Che ChangInstitute of Biomedical Sciences, Department of Life Sciences, Ph.D. Program in Translational Medicine, Rong Hsing Research Center for Translational Medicine, The iEGG and Animal Biotechnology Research Center, National Chung Hsing University, Taichung City, Taiwan.
Yuh-Chiang ShenNational Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei City, Taiwan.
National Research Institute of Chinese Medicine · TWNational Taipei University of Nursing and Health Science · TWAsia University · TWChina Medical University · TWMackay Medical University · TWTaipei Municipal YangMing Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of effective post-stroke therapy is highly demanded. Medicarpin is a key active component of a famous Chinese herbal prescription used for post-stroke treatment in Taiwan; however, little is known about its biological effects and mechanisms of action. Herein, we implemented a murine model of cerebral ischemic/reperfusional injury-related stroke to elucidate medicarpin's neuroprotective effect. In male ICR mice 24 h after stroke induction, treatment with medicarpin (0.5 and 1.0 mg/kg, i.v.) markedly enhanced the survival rates, improved moving distance and walking area coverage, reduced brain infarction, and preserved the blood-brain barrier, supporting medicarpin's protective effect on stroke-induced injury. Immunohistochemistry analysis further revealed that medicarpin treatment decreased the expression/activation of p65NF-κB and caspase 3, especially near the infarct cortex, while promoting the expression of neurogenesis-associated proteins, including doublecortin (DCX), brain-derived neurotrophic factor (BDNF), and tyrosine receptor kinase B (TrkB). These changes of expression levels were accompanied by GSK-3 inactivation and β-catenin upregulation. Notably, pretreatment with LY294002, a PI3K inhibitor, abolished the aforementioned beneficial effects of medicarpin, illustrating an essential role of PI3K/Akt activation in medicarpin's neuroprotective and reparative activities. In vitro studies revealed that medicarpin displayed strong anti-inflammatory activity by reducing nitric oxide (NO) production in lipopolysaccharide-stimulated microglial cells (BV2) with an IC

Indexed as

Brain InjuriesBrain IschemiaNeuroprotective AgentsStrokeAnimalsAnti-Inflammatory Agentsbeta CateninBrain-Derived Neurotrophic FactorCaspase 3Disease Models, AnimalGlycogen Synthase Kinase 3MaleMiceMice, Inbred ICRPhosphatidylinositol 3-KinasesPhytoalexinsAnti-Inflammatory Agentsbeta CateninBrain-Derived Neurotrophic FactorCaspase 3Glycogen Synthase Kinase 3medicarpinNeuroprotective AgentsPhosphatidylinositol 3-KinasesPhytoalexinsProto-Oncogene Proteins c-aktPterocarpans

Identifiers

PMID35649147
PMCPMC9931010
OpenAlexW4200207700

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.