Evidence map›Paper›PMID 39684254›Full record

ArticleInternational journal of molecular sciences2024

Paeoniflorin Inhibits the Activation of Microglia and Alleviates Depressive Behavior by Regulating SIRT1-NF-kB-NLRP3/Pyroptosis Pathway.

Xue Wang, Lili Su, Silu Liu, Zhongmei He, Jianming Li, Ying Zong, Weijia Chen, Rui Du

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

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

  1. Pooled it
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  9. Cell-Type-Specific WTAP and ALKBH5-Mediated mCNS neuroscience & therapeutics · 2026
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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

8 authors.

Xue WangCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Lili SuCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Silu LiuCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Zhongmei HeCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.ORCID 0000-0002-2694-6510
Jianming LiCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Ying ZongCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Weijia ChenCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
Rui DuCollege of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.

Funding

Jilin Province Major Science and Technology Special Project 20220304001YYJilin Province Major Science and Technology Special Project 20220304002YYJilin Province Science and Technology Department Talent Special 20240601086RC
6 · The paper itself

Abstract

Inflammation assumes a vital role in the pathogenesis of depression and in antidepressant treatment. Paeoniflorin (PF), a monoterpene glycoside analog possessing anti-inflammatory attributes, exhibits therapeutic efficacy on depression-like behavior in mice. The objective of this study was to evaluate the antidepressant effects of PF on depression elicited by the chronic unpredictable mild stress (CUMS) model and the precise neural sequence associated with the inflammatory process. In this study, we established an in vivo mouse model induced by CUMS and an in vitro BV2 cell model induced by LPS+ATP. The mechanism of PF for depression was assessed by the SIRT1 selective inhibitor EX-527. The findings demonstrated that PF significantly alleviated the damage of BV2 cells treated with LPS and ATP, inhibited the generation of ROS, up-regulated the expression of SIRT1 mRNA, and down-regulated the expression of nuclear NF-κB, p65, NLRP3, Caspase-1 and GSDMD-N in vitro. In vivo, PF mitigated the depressive-like behavior induced by CUMS, reduced the number of neurons, and decreased the secretion of pro-inflammatory factors IL-1β, IL-6, and TNF-α in the hippocampus. Immunohistochemical results indicated that PF attenuated CUMS-induced hyperactivation of microglia. Moreover, the expression level of SIRT1 in the hippocampus was augmented, while the protein levels of NF-κB, p65, NLRP3, Caspase-1, IL-1β and GSDMD-N were diminished after PF treatment. Additionally, the selective inhibition of SIRT1 attenuated the therapeutic effect of PF on depression. These results imply that PF possesses antidepressant properties that rely on SIRT1 signaling to regulate NLRP3 inflammasome inactivation.

Indexed as

DepressionGlucosidesMicrogliaMonoterpenesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisSignal TransductionSirtuin 1AnimalsAntidepressive AgentsCarbazolesCell LineDisease Models, AnimalGlycosidesMale6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideAntidepressive AgentsCarbazolesGlucosidesGlycosidesMonoterpenesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousepeoniflorinSirt1 protein, mouseSirtuin 1depressionNLRP3 inflammasomepaeoniflorinpyroptosisSIRT1

Identifiers

PMID39684254
PMCPMC11640976

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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.