Evidence map›Paper›PMID 41269393›Full record

ArticleMolecular neurobiology2025

Curcumin Ameliorates Depressive-like Behaviors by Modulating mGluR2/PGC-1α-Mediated Glutamatergic Homeostasis and Mitochondrial Function.

Liping Xu, Deyun Jiang, Lujing Yang, Conghua Ji, Rong Bai, Yirun Xu, Tian-Rui Xu

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. 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

7 authors.

Liping XuMedical School, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China.
Deyun JiangFaculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China.
Lujing YangFaculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China.
Conghua JiNeurology Department, The First People's Hospital of Yunnan Province, Kunming, 650032, People's Republic of China.
Rong BaiFaculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China.
Yirun XuFaculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China.
Tian-Rui XuFaculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, 650500, People's Republic of China. tianruixu@kust.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin (CUR), a natural polyphenolic compound from Curcuma longa L., exhibits anti-inflammatory, anti-oxidative, and antidepressant properties. However, the underlying antidepressant mechanisms of CUR remain unclear. Here, we used corticosterone (CORT) to establish the cellular injury and mouse depressive models to investigate CUR's protective activities. The neuroprotective effects of CUR on cells and antidepressant effects on mice were evaluated through a series of biochemical assays and behavior tests. Furthermore, the metabotropic glutamate receptor 2 (mGluR2) overexpression plasmid and siRNA-mGluR2 were separately transfected into PC12 cells to investigate the role of mGluR2 in CUR's neuroprotection. Additionally, a peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) inhibitor was used to confirm the mediating effect of mGluR2 on PGC-1α. Glutamatergic and mitochondrial-related parameters were also measured to validate CUR's protective mechanisms. Results showed that CUR intervention significantly normalized CORT-induced injuries in PC12 and depressive phenotypes in C57BL/6, restoring the mGluR2 and PGC-1α expressions repressed by CORT. mGluR2 knockdown blunted CUR's protection and aggravated CORT's effects, while mGluR2 overexpression alleviated CORT-induced injury, an effect abolished by PGC-1α inhibition, confirming mGluR2's functional role and dependence on the mGluR2/PGC-1α axis. Additionally, CUR normalized CORT-disturbed glutamate, reactive oxygen species (ROS), C-reactive protein (CRP), serotonin (5-HT) levels, mitochondrial membrane potential/morphology, and inhibited microglial activation/NF-κB signaling, confirming its effects in maintaining glutamatergic and mitochondrial homeostasis. In conclusion, CUR alleviated CORT-induced neuroinjury and depressive phenotypes by restoring mGluR2/PGC-1α signaling and maintaining glutamatergic homeostasis and mitochondrial function. Our work provides novel insights into CUR-mediated antidepressant mechanisms and underscores its therapeutic potential in depression.

Indexed as

Behavior, AnimalCurcuminDepressionGlutamic AcidHomeostasisMitochondriaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReceptors, Metabotropic GlutamateAnimalsAntidepressive AgentsCorticosteroneMaleMiceMice, Inbred C57BLPC12 CellsRatsAntidepressive AgentsCorticosteroneCurcuminGlutamic Acidmetabotropic glutamate receptor 2Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseReceptors, Metabotropic GlutamateCurcuminDepressionGlutamatergic homeostasisMGluR2/PGC-1α signalingMitochondrial function

Identifiers

PMID41269393

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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.