Evidence map›Paper›PMID 41015556›Full record

ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2025

Effect of retinoic acid on delayed encephalopathy after acute carbon monoxide poisoning: Role of the lncRNA

Fangling Huang, Su'e Wang, Zhengrong Peng, Xu Huang, Sufen Bai

Abstract read
In one paragraph

Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Fangling HuangDepartment of Hyperbaric Oxygen, Jiangxi Hospital (National Regional Center for Neurological Diseases), Xiangya Hospital, Central South University, Nanchang 330038. hfl915@csu.edu.cn.
Su'e WangDepartment of Preventive Medicine, Xiangya Hospital, Central South University, Changsha 410008, China.
Zhengrong PengDepartment of Hyperbaric Oxygen, Jiangxi Hospital (National Regional Center for Neurological Diseases), Xiangya Hospital, Central South University, Nanchang 330038. 13873151139@163.com.
Xu HuangDepartment of Hyperbaric Oxygen, Xiangya Hospital, Central South University, Changsha 410008.
Sufen BaiDepartment of Hyperbaric Oxygen, Xiangya Hospital, Central South University, Changsha 410008.

Funding

the Natural Science Foundation of Hunan Province 2021JJ31089the Scientific Research Project of Health Commission of Hunan Province 202203104548
6 · The paper itself

Abstract

objectivesThe neurotoxicity of carbon monoxide (CO) to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Our previous study found that retinoic acid (RA) can suppress the neurotoxic effects of CO. This study further explores, in vivo and in vitro, the molecular mechanisms by which RA alleviates CO-induced central nervous system damage.

methodsA cytotoxic model was established using the mouse hippocampal neuronal cell line HT22 and primary oligodendrocytes exposed to CO, and a DEACMP animal model was established in adult Kunming mice. Cell viability and apoptosis of hippocampal neurons and oligodendrocytes were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Annexin V/propidium iodide (PI) double staining. The transcriptional and protein expression of each gene was detected using real-time fluorescence quantitative PCR (RT-qPCR) and Western blotting. Long noncoding RNA (lncRNA)

resultsRA at 10 and 20 μmol/L significantly reversed CO-induced apoptosis of hippocampal neurons and oligodendrocytes, downregulation of

conclusionsRA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes, thereby reducing central nervous system injury and exerting neuroprotective effects. LncRNA

Indexed as

Brain-Derived Neurotrophic FactorBrain DiseasesCarbon Monoxide PoisoningMembrane ProteinsNerve Tissue ProteinsRNA, Long NoncodingTretinoinAnimalsApoptosisCell LineHippocampusMaleMiceNeuronsOligodendrogliaReceptor, trkBBdnf protein, mouseBrain-Derived Neurotrophic FactorMembrane ProteinsNerve Tissue ProteinsReceptor, trkBRNA, Long NoncodingTretinoinapoptosisdelayed encephalopathy after acute carbon monoxide poisoningLINGO-1lncRNA SNHG15neuroprotectionretinoic acid

Identifiers

PMID41015556
PMCPMC12464924

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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.