Evidence map›Paper›PMID 33907032›Full record

ArticleNeural regeneration research2021

Protein profiling identified mitochondrial dysfunction and synaptic abnormalities after dexamethasone intervention in rats with traumatic brain injury.

Fei Niu, Bin Zhang, Jie Feng, Xiang Mao, Xiao-Jian Xu, Jin-Qian Dong, Bai-Yun Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 52% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Brain Proteomic Responses to Glucocorticoids and Their Relationship With Transcriptome: A Systematic Meta-Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Pooled it
  2. Article
  3. Review
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

7 authors at 3 institutions in 1 country.

Fei NiuDepartment of Neurotrauma, Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Bin ZhangDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Jie FengKey Laboratory of Central Nervous System Injury Research, Center for Brain Tumor, Beijing Institute of Brain Disorders, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Xiang MaoDepartment of Neurosurgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China.
Xiao-Jian XuDepartment of Neurotrauma, Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
Jin-Qian DongDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Bai-Yun LiuDepartment of Neurotrauma, Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute; Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University; Center for Nerve Injury and Repair, Beijing Institute of Brain Disorders; China National Clinical Research Center for Neurological Diseases, Beijing, China.
Capital Medical University · CNBeijing Tian Tan Hospital · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability, inhibit free radicals, and reduce cerebrospinal fluid production. According to the latest guidelines for the treatment of traumatic brain injury in the United States, high-dose glucocorticoids cause neurological damage. To investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect, rat controlled cortical impact models of traumatic brain injury were established. At 1 hour and 2 days after surgery, rat models were intraperitoneally administered dexamethasone 10 mg/kg. The results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone treatment. The Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling pathway. Western blot analysis and immunohistochemistry results showed that Ndufv2, Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model group. These findings suggest that dexamethasone may promote a compensatory increase in complex I subunits (Ndufs2 and Ndufv2), increase the expression of mitochondrial enzyme Maob, and upregulate synaptic-transmission-related protein Gria3. These changes may be caused by nerve injury after traumatic brain injury treatment by dexamethasone. The study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute (approval No. 201802001) on June 6, 2018.

Indexed as

dexamethasoneGria3Maobmass spectrometrymitochondrial dysfunctionNdufs2Ndufv2proteomicssynaptic abnormalitiestraumatic brain injury

Identifiers

PMID33907032
PMCPMC8374556
OpenAlexW3158845454

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.