Evidence map›Paper›PMID 35338452›Full record

ArticleMolecular neurobiology2022

lncRNA BDNF-AS Attenuates Propofol-Induced Apoptosis in HT22 Cells by Modulating the BDNF/TrkB Pathway.

Yu-Hai Xu, Yuan Luo, Jiang-Bei Cao, Yan-Hong Liu, Yu-Xiang Song, Xiao-Ying Zhang, Qiang Fu, Wei-Dong Mi, Hao Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Yu-Hai Xu1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China.
Yuan LuoAir Force Medical Center, PLA, 30th Fucheng Road, Haidian District, Beijing, 100142, China.
Jiang-Bei Cao1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China.
Yan-Hong Liu1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China.
Yu-Xiang Song1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China.
Xiao-Ying Zhang1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China.
Qiang Fu1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China. 13691436328@163.com.
Wei-Dong Mi1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China. wwdd1962@aliyun.com.
Hao Li1st Medical Center of Chinese PLA General Hospital, 28th Fuxing Road, Haidian District, Beijing, 100853, China. lihao301@126.com.ORCID http://orcid.org/0000-0002-9759-2537
Chinese PLA General Hospital · CNAir Force General Hospital PLA · CN

Funding

Beijing Science and Technology New Star Program Z181100006218073the Military Medical Technology Incubation Project for Youth 20QNPY094the Natural Science Foundation of China 81901097
6 · The paper itself

Abstract

Propofol is widely used as an intravenous anesthetic in clinical practice. Previous studies have indicated that propofol induces apoptosis in neurons. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, is associated with neuronal apoptosis. BDNF-AS, a relatively conserved long non-coding RNA, can reverse the transcription of BDNF. This study aimed to investigate the involvement of BDNF-AS in propofol-induced apoptosis in HT22 cells. HT22 cells were treated with various concentrations of propofol at different time points. BDNF-AS was silenced using BDNF-AS-targeting siRNA. TrkB was antagonized by the TrkB inhibitor, ANA-12. Flow cytometry, quantitative reverse-transcription PCR, and western blotting were performed to analyze apoptosis and the expression of genes and proteins, respectively. In propofol-treated HT22 cells, BDNF-AS was upregulated, and BDNF was downregulated in a time- and dose-dependent manner. BDNF-AS downregulation mediated by siRNA mitigated apoptosis, upregulated the expression of Bcl-2, and downregulated the expression of Bax and caspase-3, 7, and 9. ANA-12 downregulated the expression of Bcl-2, upregulated the expression of Bax and caspase-3, 7, and 9, and increased apoptosis. Our study implied that inhibition of BDNF-AS can decrease propofol-induced apoptosis by activating the BDNF/TrkB pathway. Thus, the BDNF-AS-BDNF/TrkB signaling pathway may be a valuable target for treating propofol-induced neurotoxicity.

Indexed as

PropofolRNA, Long NoncodingApoptosisbcl-2-Associated X ProteinBrain-Derived Neurotrophic FactorCaspase 3Receptor, trkBRNA, Small Interferingbcl-2-Associated X ProteinBrain-Derived Neurotrophic FactorCaspase 3PropofolReceptor, trkBRNA, Long NoncodingRNA, Small InterferingApoptosisBDNF-ASHippocampuslncRNAPropofol

Identifiers

PMID35338452
PMCPMC9148285
OpenAlexW4221135263

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.