Evidence map›Paper›PMID 40469980›Full record

ArticleFrontiers in pharmacology2025

Sinisan ameliorates early-life stress-induced depressive-like behaviors by repairing DRN synaptic damage through CaSR.

Qingying Yu, Huan Li, Xulan Cui, Liuchang Zhou, Zedan Xie, Shanshan Wang, Di Deng, Jinlan Zhao, Peng Sun, Yafei Shi and 1 more

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. 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. Article
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

11 authors.

Qingying YuGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Huan LiGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Xulan CuiGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Liuchang ZhouGuangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Zedan XieGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Shanshan WangGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Di DengGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Jinlan ZhaoGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Peng SunInnovation Research Institute of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Yafei ShiSchool of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Rong ZhangGuangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indroduction: Early-life stress (ELS) is a well-established risk factor for adolescent depression, yet the underlying neurobiological mechanisms remain incompletely understood. The dorsal raphe nucleus (DRN), a key serotonergic center, demonstrates stress-induced synaptic impairments that may underlie depressive phenotypes. Sinisan (SNS), a classical Chinese herbal formula, shows clinical efficacy against mood disorders, but its effects on adolescent stress-induced DRN synaptic damage are unknown. Methods: Using a maternal separation plus chronic unpredictable mild stress (MSCUMS) model in adolescent rats, we integrated behavioral tests with various neurobiological analyses. Depressive-like behaviors were evaluated, synaptic ultrastructure in the DRN was examined via electron microscopy, and CaSR expression was measured. The therapeutic effects of SNS and the mechanistic role of CaSR were investigated through pharmacological activation (GdCl3). Results: MS-CUMS induced: (1) depressive-like behaviors, (2) DRN synaptic ultrastructural damage, and (3) Calcium-sensing receptor (CaSR) downregulation. SNS treatment normalized depression/anxiety behaviors, restored CaSR expression and ameliorated synaptic damage. CaSR activation (GdCl3) reversed these deficits, confirming its mechanistic role. Discussion: These results demonstrate that CaSR mediates ELS-induced DRN synaptic impairment, and SNS exerts rapid antidepressant effects via CaSR upregulation.

Indexed as

calcium-sensitive receptorsdepressiondorsal raphe nucleusSNSsynaptic structure

Identifiers

PMID40469980
PMCPMC12133890

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