Evidence map›Paper›PMID 29357017›Full record

ArticleNeurochemical research2018

Berberine Ameliorates MCAO Induced Cerebral Ischemia/Reperfusion Injury via Activation of the BDNF-TrkB-PI3K/Akt Signaling Pathway.

Jun Yang, Hui Yan, Sumei Li, Min Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  3. A Small-Molecule Activator of Sarco/Endoplasmic Reticulum CaACS pharmacology & translational science · 2025
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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

4 authors at 1 institution in 1 country.

Jun YangDepartment of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.
Hui YanDepartment of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.
Sumei LiDepartment of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China.
Min ZhangDepartment of Neurology, Affiliated Hospital of Jining Medical University, 89 guhuai Road, Jining, 272000, Shandong, People's Republic of China. sdmzhangming@126.com.
Affiliated Hospital of Jining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemic injury remains associated with high mortality rates and lacks effective therapeutic intervention. Berberine (BBR) possesses anti-oxidant, anti-inflammatory, and anti-tumor activities, as well as potent neuroprotective effects. Although recent studies have examined the neuroprotective effects of berberine, little is known regarding its usefulness in treating cerebral ischemia. Thus, the aim of this study is to investigate the possible effect and the mechanism of berberine against cerebral ischemic injury using the middle cerebral artery occlusion (MCAO) model. Rats were randomly divided into three groups: control group, MCAO group, and MCAO + BBR group. Modified neurological severity score tests (mNSS) and infarct volumes were measured to determine the neuroprotective effects of berberine. Neuronal survival in striatum was examined by TUNEL staining and immunohistochemistry. Western blotting measured the expression of BDNF, TrkB, p-Akt and cleaved caspase-3. The results demonstrated that BBR could significantly protect against MCAO. Berberine also increased the expression of BDNF, TrkB, and p-Akt, which were reduced after MCAO. Furthermore, treatment with BBR declined the apoptosis-related proteins induced by MCAO. However, treatment with LY294002 (PI3K inhibitor) reversed the BBR-induced increases in BDNF and p-Akt proteins and decreased cleaved caspase-3 protein expression in focal cerebral ischemic rats. In summary, our results demonstrated that BBR could exert neuroprotective effects through reduction of striatum apoptosis via the BDNF-TrkB-PI3K/Akt signaling pathway.

Indexed as

AnimalsApoptosisBerberineBrain-Derived Neurotrophic FactorBrain IschemiaInfarction, Middle Cerebral ArteryMaleNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRats, Sprague-DawleyReperfusion InjuryBerberineBrain-Derived Neurotrophic FactorNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisBDNFBerberineMCAOPI3K/AktTrkB

Identifiers

PMID29357017
OpenAlexW2792377060

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.