Evidence map›Paper›PMID 30686973›Full record

ArticleFrontiers in neuroscience2018

Baicalin Protects Mice Brain From Apoptosis in Traumatic Brain Injury Model Through Activation of Autophagy.

Jiang Fang, Yihao Zhu, Handong Wang, Bailu Cao, Maoxing Fei, Wenhao Niu, Yuan Zhou, Xiaoliang Wang, Xiang Li, Mengliang Zhou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.3field-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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. Article
  7. Article
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  10. Anti-inflammatory effect of baicalin in rats with adjuvant arthritis and its autophagy- related mechanism.Technology and health care : official journal of the European Society for Engineering and Medicine · 2022
    Article
  11. Review
  12. Article
  13. Article
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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

10 authors at 4 institutions in 1 country.

Jiang FangDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Yihao ZhuDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Handong WangDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Bailu CaoJinling Clinical Medical College, Nanjing Medical University, Nanjing, China.
Maoxing FeiDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Wenhao NiuDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Yuan ZhouDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Xiaoliang WangDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Xiang LiDepartment of Neurosurgery, Jiangsu Provincial Second Chinese Medicine Hospital, Nanjing, China.
Mengliang ZhouDepartment of Neurosurgery, Jinling Hospital, Nanjing, China.
Nanjing General Hospital of Nanjing Military Command · CNJinling Institute of Technology · CNNanjing University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is associated with secondary injury following traumatic brain injury (TBI) and is expected to be a therapeutic target. Baicalin, a neuroprotective agent, has been proven to exert multi-functional bioactive effects in brain injury diseases. However, it is unknown if Baicalin influences autophagy after TBI. In the present study, we aimed to explore the effects that Baicalin had on TBI in a mice model, focusing on autophagy as a potential mechanism. We found that Baicalin administration significantly improved motor function, reduced cerebral edema, and alleviated disruption of the blood-brain barrier (BBB) after TBI in mice. Besides, TBI-induced apoptosis was reversed by Baicalin evidenced by Nissl staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and the level of cleaved caspase-3. More importantly, Baicalin enhanced autophagy by detecting the autophagy markers (LC3, Beclin 1, and p62) using western blot and LC3 immunofluorescence staining, ameliorating mitochondrial apoptotic pathway evidenced by restoration of the TBI-induced translocation of Bax and cytochrome C. However, simultaneous treatment with 3-MA inhibited Baicalin-induced autophagy and abolished its protective effects on mitochondrial apoptotic pathway. In conclusion, we demonstrated that Baicalin enhanced autophagy, ameliorated mitochondrial apoptosis and protected mice brain in TBI mice model.

Indexed as

apoptosisautophagyBaicalinmitochondrial apoptosistraumatic brain injury

Identifiers

PMID30686973
PMCPMC6334745
OpenAlexW2909559247

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Registered trials

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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.