Evidence map›Paper›PMID 41914021›Full record

ArticleCNS neuroscience & therapeutics2026

Panacis Quinquefolii Radix Polysaccharides Alleviate Depressive-Like Behaviors in Chronic Unpredictable Mild Stress-Induced Mice by Suppressing Complement C1Q/C3-Mediated Microglial Synaptic Pruning and Modulating Gut Microbiota.

Mengjun Xie, Lingling Feng, Ruyi Li, Mengqi Li, Liang Shen, Minghui Zhang, Yutong Wei, Qiao Yin, Datong Wang, Liqing Chen and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Mengjun XieJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Lingling FengJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Ruyi LiDepartment of Marine Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Mengqi LiJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Liang ShenJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Minghui ZhangDepartment of Marine Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
Yutong WeiJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Qiao YinDepartment of Neurology, Clinical Research Center of Neurological Disease, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Datong WangJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.
Liqing ChenJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Kai SongDepartment of Nephrology, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Peipei WangDepartment of Marine Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.ORCID https://orcid.org/0000-0001-6880-6084
Qifei CongJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases, Institute of Neuroscience, Soochow University, Suzhou, China.ORCID https://orcid.org/0000-0002-4446-7222

Funding

Jiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases KJS2546Key Project of the Natural Science Foundation of Jiangsu Provincial Higher Education Institutions 25KJA310003National Natural Science Foundation of China 32200778National Natural Science Foundation of China 32471014Natural Science Foundation of Jiangsu Province BK20220494Priority Academic Program Development of Jiangsu Higher Education InstitutesProject of Biomedical Basic Research Center of JiangsuProject of MOE Key Laboratory of Geriatric Diseases and Immunology KJS2501Scientific Research Project of Jiangsu Association of Chinese Medicine ZXF2024072State Key Laboratory of Drug Research, Chinese Academy of Sciences SKLDR-2023-KF-05Suzhou International Joint Laboratory for Diagnosis and Treatment of Brain DiseasesSuzhou Medical and Health Technology Innovation Project SKY2022107Young Science Talents Promotion Project of Jiangsu Science and Technology Association TJ-2023-019
6 · The paper itself

Abstract

aimsPanax quinquefolius Radix (American ginseng) is a medicinal herb used for its neuroprotective and tonic effects. However, the antidepressant potential of its polysaccharide components is not well studied. This research aimed to investigate the antidepressant effects of XYS1, a polysaccharide from American ginseng, focusing on mechanisms related to the complement system and the gut-brain axis.

methodsA chronic unpredictable mild stress (CUMS) mouse model was used to induce depressive behaviors. Mice were treated with XYS1 via oral gavage, followed by assessments of behavior, molecular changes, and gut microbiota.

resultsXYS1 treatment significantly alleviated depression-like behaviors in CUMS mice, as demonstrated by reduced immobility time in the TST and FST, and increased sucrose preference and body weight. Mechanistically, XYS1 attenuated complement system activation by downregulating C1Q expression in microglia and C3 expression in astrocytes, not only in the hippocampal CA1 region but also in the mPFC and PVN, as well as in the colon. Furthermore, XYS1 inhibited microglial activation and associated synaptic phagocytosis, preserved glutamatergic neuron density, restored excitatory synapse density, and reversed CUMS-induced gut microbiota dysbiosis by enriching Bacillota and reducing Bacteroidota abundance. Additionally, XYS1 effectively mitigated both colonic and systemic inflammation, reducing pro-inflammatory cytokines TNF-α and IL-1β and complement components C1Q and C3, while restoring anti-inflammatory IL-10 levels, thereby modulating the gut-brain axis.

conclusionsXYS1 exerts antidepressant effects by modulating the C1Q/C3 complement pathway, inhibiting microglial-mediated synaptic pruning, and restoring gut microbiota homeostasis.

Indexed as

Antidepressive AgentsComplement C1qComplement C3DepressionGastrointestinal MicrobiomeMicrogliaNeuronal PlasticityPanaxPolysaccharidesStress, PsychologicalAnimalsMaleMiceMice, Inbred C57BLAntidepressive AgentsComplement C1qComplement C3Polysaccharideschronic unpredictable mild stresscomplementgut microbiotamicrogliaPanacis Quinquefolii Radixpolysaccharide

Identifiers

PMID41914021
PMCPMC13140852

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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.