Evidence map›Paper›PMID 30127597›Full record

ArticleDrug design, development and therapy2018

Baicalin provides neuroprotection in traumatic brain injury mice model through Akt/Nrf2 pathway.

Jiang Fang, Handong Wang, Jian Zhou, Wei Dai, Yihao Zhu, Yuan Zhou, Xiaoliang Wang, Mengliang Zhou

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 105 citations in OpenAlex.

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  13. Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
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  18. AIMS neuroscience · 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

8 authors at 3 institutions in 1 country.

Jiang FangDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Southeast University, Nanjing, China, njhdwang@hotmail.com.
Handong WangDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Southeast University, Nanjing, China, njhdwang@hotmail.com.
Jian ZhouDepartment of Neurosurgery, Jinling Hospital, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, China.
Wei DaiDepartment of Neurosurgery, Jinling Hospital, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, China.
Yihao ZhuDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Yuan ZhouDepartment of Neurosurgery, Jinling Hospital, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, China.
Xiaoliang WangDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Mengliang ZhouDepartment of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Jinling Institute of Technology · CNNanjing General Hospital of Nanjing Military Command · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe neuroprotective effects of Baicalin have been confirmed in several central nervous system (CNS) diseases. However, its possible effect on traumatic brain injury (TBI) model is still not clear. The present study is aimed to investigate the role and the underling mechanisms of 7-D-glucuronic acid-5,6-dihydroxyflavone (Baicalin) on TBI model.

methodsThe weight-drop model of TBI in Institute of Cancer Research mice was treated with Baicalin intraperitoneally at 30 minutes after TBI. LY294002 (LY) (a commonly used PI3K/Akt pathway inhibitor) was injected into the left ventricle at 30 minutes before TBI. All mice were euthanized at 24 hours after TBI to collect the brain tissue for a series of tests except for neurological function, which was measured at 2 hours and 1 and 3 days post-TBI.

resultsBaicalin administration significantly improved neurobehavioral function, alleviated brain edema, and reduced apoptosis-positive cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay accompanied with the upregulation of B-cell lymphoma 2 (Bcl-2) and downregulation of Bcl-2-associated X protein (Bax) and cleaved-caspase 3 by Western blot. Besides, TBI-induced oxidant stress status was also restored in the Baicalin group by measuring malondialdehyde (MDA) content, glutathione peroxidase (GPx), and superoxide dismutase (SOD) levels in the injured brain cortex. Furthermore, translocation of Nrf2 to the nucleus was dramatically enhanced by Baicalin verified by immunofluorescence and Western blot analyses. Accordingly, its downstream antioxidative enzymes nicotinamide adenine dinucleotide phosphate:quinine oxidoreductase 1 (NQO-1) and heme oxygenase 1 (HO-1) were also activated by Baicalin confirmed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot. However, cotreatment with Baicalin and LY could partly abolish Baicalin-induced activation of Nrf2 and its neuroprotective effects in TBI.

conclusionThis study demonstrates that Baicalin provides a neuroprotective effect in TBI mice model via activating the Akt/Nrf2 pathway.

Indexed as

Active Transport, Cell NucleusAnimalsApoptosisApoptosis Regulatory ProteinsBehavior, AnimalBrainBrain EdemaBrain Injuries, TraumaticDisease Models, AnimalFlavonoidsMaleMice, Inbred ICRNeuronsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressApoptosis Regulatory ProteinsbaicalinFlavonoidsNeuroprotective AgentsNfe2l2 protein, mouseNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktAktapoptosisBaicalinnuclear factor erythroid 2-related factor 2oxidative stresstraumatic brain injury

Identifiers

PMID30127597
PMCPMC6089097
OpenAlexW2885861652

What OpenQuestion holds

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LicenceCC BY-NC
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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.