Evidence map›Paper›PMID 38411637›Full record

ArticlePsychopharmacology2024

Calcitriol attenuates lipopolysaccharide-induced neuroinflammation and depressive-like behaviors by suppressing the P2X7R/NLRP3/caspase-1 pathway.

Changshui Wang, Changmeng Cui, Xin Xie, Beibei Chen, Lei Feng, Pei Jiang

Abstract read
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In one paragraph

Article in Psychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
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

4 citing papers in PubMed, 14 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Changshui WangDepartment of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, China.
Changmeng CuiDepartment of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, China.
Xin XieInstitute of Translational Pharmacy, Jining Medical Research Academy, Jining, China.
Beibei ChenInstitute of Translational Pharmacy, Jining Medical Research Academy, Jining, China.
Lei FengDepartment of Neurosurgery, Jining First People's Hospital, Shandong First Medical University, Jining, China. fengleineuros@sina.com.
Pei JiangInstitute of Translational Pharmacy, Jining Medical Research Academy, Jining, China. jiangpeicsu@sina.com.ORCID http://orcid.org/0000-0002-8360-7427
Jining First People's Hospital · CNAffiliated Hospital of Jining Medical University · CN

Funding

China International Medical Foundation Z-2018-35-2002High-Level Research Project Fostering Plan of Jining Medical University JYGC2021FKJ009Key Research and Development Projects of Jining City 2019MNS012Key Research and Development Projects of Jining City 2021YXNS084National Natural Science Foundation of China 81602846Natural Science Foundation of Shandong Province ZR2020MH375Natural Science Foundation of Shandong Province ZR2021MH145Natural Science Foundation of Shandong Province ZR2023MH365Project Foundation of Affiliated Hospital of Jining Medical University MP-ZD-2021-005
6 · The paper itself

Abstract

rationaleMicroglia-mediated neuroinflammation is a vital hallmark in progression of depression, while calcitriol exerts anti-inflammatory effects in the brain. The activation of the P2X7 receptor has an important link to neuroinflammation. However, it is unclear whether calcitriol treatment exerts anti-inflammatory effects in association with P2X7R activation.

objectiveIn this study, we assessed the antidepressive and neuroprotective effects of calcitriol on lipopolysaccharide (LPS)-mediated depressive-like behavior, neuroinflammation, and neuronal damage.

methodsIn in vitro experiments, the BV2 cells were exposed to LPS, and the protective effects of calcitriol were assessed. For in vivo experiment, thirty-two male C57BL/6 mice were divided into four groups of control, calcitriol, LPS and LPS + calcitriol. Calcitriol was administered at 1 µg/kg for 14 days and LPS at 1 mg/kg once every other day for 14 days. The control group mice were given equal volumes of vehicles. All treatments were delivered intraperitoneally.

resultsThe in vitro experiments showed calcitriol inhibited the release of inflammatory mediators induced by LPS in BV2 cells. The in vivo experiments revealed that calcitriol alleviated LPS-induced behavioral abnormalities and spatial learning impairments. Moreover, calcitriol treatment reduced the mRNA levels of pro-inflammatory cytokines, while increasing anti-inflammatory cytokine levels in the hippocampus. Our results further revealed that calcitriol administration attenuated LPS-induced microglia activation by suppressing P2X7R/NLRP3/caspase-1 signaling. Moreover, calcitriol inhibited apoptosis of neurons in the hippocampus as evidenced by expression of apoptosis-related proteins and TUNEL assay.

conclusionsCollectively, our findings demonstrated that calcitriol exerts antidepressive and neuroprotective effects through the suppression of the P2X7R/NLRP3/caspase-1 pathway both in LPS-induced inflammation models in vitro and in vivo.

Indexed as

CalcitriolCaspase 1DepressionLipopolysaccharidesMice, Inbred C57BLMicrogliaNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Purinergic P2X7AnimalsAntidepressive AgentsAnti-Inflammatory AgentsBehavior, AnimalCell LineDisease Models, AnimalHippocampusAntidepressive AgentsAnti-Inflammatory AgentsCalcitriolCasp1 protein, mouseCaspase 1LipopolysaccharidesNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReceptors, Purinergic P2X7CalcitriolDepressionNeuroinflammationNLRP3 inflammasomeP2X7R

Identifiers

PMID38411637
OpenAlexW4392194351

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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.