Evidence map›Paper›PMID 37322430›Full record

ArticleBMC complementary medicine and therapies2023

A whole transcriptome profiling analysis for antidepressant mechanism of Xiaoyaosan mediated synapse loss via BDNF/trkB/PI3K signal axis in CUMS rats.

Pan Meng, Xi Zhang, Tong-Tong Liu, Jian Liu, Yan Luo, Ming-Xia Xie, Hui Yang, Rui Fang, Dong-Wei Guo, Zi-Yan Zhong and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  8. E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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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

12 authors at 4 institutions in 1 country.

Pan MengHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China.
Xi ZhangThe Second People's Hospital of Hunan Province, Changsha, Hunan, China.
Tong-Tong LiuHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China.
Jian LiuFirst Affiliated Hospital, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Yan LuoHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China.
Ming-Xia XieHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China.
Hui YangFirst Affiliated Hospital, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Rui FangHunan Academy of Chinese Medicine, Yuelu District, 58 Lushan Road, Changsha, Hunan, China.
Dong-Wei GuoThe Second People's Hospital of Hunan Province, Changsha, Hunan, China.
Zi-Yan ZhongHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China.
Yu-Hong WangHunan University of Chinese Medicine, 300 Xueshi Road, Hanpu Science and Education Park, Yuelu District, Hunan, Changsha, China. wyh_107@163.com.
Jin-Wen GeHunan Academy of Chinese Medicine, Yuelu District, 58 Lushan Road, Changsha, Hunan, China. 001267@hnucm.edu.cn.
Hunan University of Traditional Chinese Medicine · CNFirst Affiliated Hospital of Hunan University of Traditional Chinese Medicine · CNHunan Academy of Traditional Chinese Medicine · CNSecond People Hospital of Hunan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDepression is a neuropsychiatric disease resulting from deteriorations of molecular networks and synaptic injury induced by stress. Traditional Chinese formula Xiaoyaosan (XYS) exert antidepressant effect, which was demonstrated by a great many of clinical and basic investigation. However, the exact mechanism of XYS has not yet been fully elucidated.

methodsIn this study, chronic unpredictable mild stress (CUMS) rats were used as a model of depression. Behavioral test and HE staining were used to detect the anti-depressant effects of XYS. Furthermore, whole transcriptome sequencing was employed to establish the microRNA (miRNA), long non-coding RNA (lncRNA), circular RNA (circRNA), and mRNA profiles. The biological functions and potential mechanisms of XYS for depression were gathered from the GO and KEGG pathway. Then, constructed the competing endogenous RNA (ceRNA) networks to illustrate the regulatory relationship between non-coding RNA (ncRNA) and mRNA. Additionally, longest dendrite length, total length of dendrites, number of intersections, and density of dendritic spines were detected by Golgi staining. MAP2, PSD-95, SYN were detected by immunofluorescence respectively. BDNF, TrkB, p-TrkB, PI3K, Akt, p-Akt were measured by Western Blotting.

resultsThe results showed that XYS could increase the locomotor activity and sugar preference, decreased swimming immobility time as well as attenuate hippocampal pathological damage. A total of 753 differentially expressed lncRNAs (DElncRNAs), 28 circRNAs (DEcircRNAs), 101 miRNAs (DEmiRNAs), and 477 mRNAs (DEmRNAs) were identified after the treatment of XYS in whole transcriptome sequencing analysis. Enrichment results revealed that XYS could regulate multiple aspects of depression through different synapse or synaptic associated signal, such as neurotrophin signaling and PI3K/Akt signaling pathways. Then, vivo experiments indicated that XYS could promote length, density, intersections of synapses and also increase the expression of MAP2 in hippocampal CA1, CA3 regions. Meanwhile, XYS could increase the expression of PSD-95, SYN in the CA1, CA3 regions of hippocampal by regulating the BDNF/trkB/PI3K signal axis.

conclusionThe possible mechanism on synapse of XYS in depression was successfully predicted. BDNF/trkB/PI3K signal axis were the potential mechanism of XYS on synapse loss for its antidepressant. Collectively, our results provided novel information about the molecular basis of XYS in treating depression.

Indexed as

Brain-Derived Neurotrophic FactorPhosphatidylinositol 3-KinasesAnimalsAntidepressive AgentsDrugs, Chinese HerbalProto-Oncogene Proteins c-aktRatsSynapsesAntidepressive AgentsBrain-Derived Neurotrophic FactorDrugs, Chinese HerbalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktxiaoyaosanBDNF/trkB/PI3K signal axisDepressionSynapse lossWhole transcriptomic analysisXiaoyaosan

Identifiers

PMID37322430
PMCPMC10273699
OpenAlexW4380870426

What OpenQuestion holds

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LicenceCC BY
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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.