Evidence map›Paper›PMID 39611999›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2025

Tauroursodeoxycholic acid mitigates depression-like behavior and hippocampal neuronal damage in a corticosterone model of female mice.

Wei Shen, Zikang Li, Yanlin Tao, Houyuan Zhou, Hui Wu, Hailian Shi, Fei Huang, Xiaojun Wu

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
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  4. Review
  5. 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

8 authors.

Wei Shen *Shanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Zikang Li *Shanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Yanlin TaoShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Houyuan ZhouShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Hui WuShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Hailian ShiShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Fei HuangShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China. Fei_H@hotmail.com.
Xiaojun WuShanghai Key Laboratory of Compound Chinese Medicines, the Ministry of Education (MOE) Key Laboratory for Standardization of Chinese Medicines, the MOE Innovation Centre for Basic Medicine Research On Qi-Blood TCM Theories, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China. xiaojunwu320@126.com.

Funding

Natural Science Foundation of Shanghai Municipality 21ZR1460600
6 · The paper itself

Abstract

Depression, a complex mental disorder influenced by both psychological and physiological factors, predominantly affects females. Studies have indicated that elevated levels of cortisol/corticosterone (CORT) under stress conditions can lead to hippocampal neuronal damage, thereby contributing to depression. Tauroursodeoxycholic acid (TUDCA), a bile acid, possesses anti-apoptotic, antioxidant, and anti-inflammatory properties. This study aimed to investigate the protective mechanism of TUDCA against CORT-induced neuromolecular and behavioral phenotypes of depression in female mice, providing theoretical support for its use in treating female depression. The antidepressant effects of TUDCA were evaluated through a series of behavioral tests, measurement of serum neurotransmitter levels, Nissl staining of the hippocampal CA3 region, and assessment of hippocampal proteins. Behavioral results demonstrated that TUDCA exhibited antidepressant effects, as evidenced by increased sucrose preference and locomotor activity, as well as reduced immobility time in depressed mice. Furthermore, TUDCA ameliorated neurotransmitter imbalances. Nissl staining revealed that TUDCA reduced neuronal damage in depressed mice, while Western blotting results indicated that TUDCA activated the hippocampal BDNF/TrkB/CREB pathway and regulated the expression of GR-related proteins. These findings suggested that TUDCA exerted neuroprotective effects in CORT-induced neuronal damage in female depressed mice. The mechanism appeared to be related to the activation of the BDNF/TrkB/CREB signaling pathway and the modulation of GR-related protein expression.

Indexed as

Antidepressive AgentsBehavior, AnimalDepressionHippocampusNeuronsNeuroprotective AgentsTaurochenodeoxycholic AcidAnimalsBrain-Derived Neurotrophic FactorCorticosteroneCyclic AMP Response Element-Binding ProteinDisease Models, AnimalFemaleMiceReceptor, trkBAntidepressive AgentsBdnf protein, mouseBrain-Derived Neurotrophic FactorCorticosteroneCyclic AMP Response Element-Binding ProteinNeuroprotective AgentsNtrk2 protein, mouseReceptor, trkBTaurochenodeoxycholic AcidursodoxicoltaurineCorticosteroneDepressionFemaleHippocampal neuronsTauroursodeoxycholic acid

Identifiers

What Socratic holds

Textmetadata
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Registered trials

None linked

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 Socratic graph.