Evidence map›Paper›PMID 40281108›Full record

ArticleScientific reports2025

Rinsenoside Rg1 and its involvement in Hippo-YAP signaling pathway alleviating symptoms of depressive-like behavior.

Linyin Gao, Jiarong Wang, Xiuchang Liu, Lei Wu, Ran Ding, Xuemei Han, Xindi Wang, Hao Ma, Jie Pan, Xiujun Zhang and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
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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.

Linyin Gao *Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Jiarong Wang *School of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Xiuchang Liu *Key Laboratory of RNA Science and Engineering, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang District, Beijing, 100101, China.
Lei WuSchool of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Ran DingHebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Xuemei HanHebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Xindi WangHebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Hao MaHebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Jie PanSchool of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China.
Xiujun ZhangSchool of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China. zhxj@ncst.edu.cn.
Haitao WangSchool of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China. wht92725@163.com.
Xueliang ShangSchool of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, 063210, Hebei, China. shangxuelianghao@126.com.

Funding

Medical Science Research Project of Hebei Province in 2023 20231585STI2030-Major Projects 2021ZD0200700the central government guides local science and technology development fund project 246Z2511G, 246Z2605Gthe key project of Hebei Natural Science Foundation Chinese Medicine Joint Fund H2022209080the key research project of North China University of Science and Technology in 2023 ZD-YG-202314-23the research project of basic scientific research service fees in provincial universities of North China University of Technology JQN2023039
6 · The paper itself

Abstract

Ginsenoside Rg1 (G-Rg1) has potential antidepressant effects, but the underlying mechanism remains unclear. Presently, sixty 6-8 week-old male C57BL/6 mice were selected and randomly allocated to control, chronic restraint stress (CRS), CRS and low G-Rg1 administration (CRS + L-Rg1), CRS and high G-Rg1 administration (CRS + H-Rg1), and CRS and fluoxetine administration (CRS + FLX) groups. The component of anxiety in psychic processes and neuropathological changes occurring in dentate gyrus (DG) neurons were evaluated, where PC12 cells were assessed for the expression of G-Rg1. Both cell viability and apoptosis were analyzed. G-Rg1 (5 and 10 mg/kg/day) alleviated the behavioral manifestations of neuropathological processes revealed in DG neurons of CRS-induced mice. Western blotting analysis demonstrated the negative correlation of G-Rg1 level and that of Hipp-YAP signaling pathway components including p-YAP/YAP, p-MST1/MST1, and p-LATS1/LATS1, which were triggered by CRS. Combined therapy with G-Rg1 (10 mM) proved to have an inhibitory effect on PC12 cell viability and apoptosis compared to sole cort treatment. In addition, chronic G-Rg1 also reduced the protein expression levels of Hippo-YAP signaling pathway activated by corticosterone (Cort) including p-YAP/YAP, p-MST1/MST1, and p-LATS1/LATS1. The above mentioned improvements could be implemented due to XMU-MP-1 hampering the processes in Hippo-YAP signaling pathway. Importantly, the changes in synaptic plasticity and apoptosis were thoroughly investigated to determine the role of chronic G-Rg1 in the forementioned processes. In conclusion, chronic G-Rg1 played an important neuroprotective role in either CRS mice or Cort-treated cells associated with the inhibition of Hippo-YAP signaling pathway, which was the core part of decreasing neuronal apoptosis and enhancing synaptic plasticity.

Indexed as

Adaptor Proteins, Signal TransducingAntidepressive AgentsDepressionGinsenosidesProtein Serine-Threonine KinasesSignal TransductionAnimalsApoptosisBehavior, AnimalCell Cycle ProteinsCell SurvivalDentate GyrusDisease Models, AnimalHippo Signaling PathwayMaleMiceAdaptor Proteins, Signal TransducingAntidepressive AgentsCell Cycle Proteinsginsenoside Rg1GinsenosidesProtein Serine-Threonine KinasesYap1 protein, mouseYAP-Signaling ProteinsApoptosisDepressionGinsenoside Rg1Hippo-YAP signaling pathwaySynaptic plasticity

Identifiers

PMID40281108
PMCPMC12032003

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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.