Evidence map›Paper›PMID 32833187›Full record

ArticleMolecular neurobiology2020

Nobiletin Ameliorates NLRP3 Inflammasome-Mediated Inflammation Through Promoting Autophagy via the AMPK Pathway.

Haidong Wang, Yujin Guo, Yi Qiao, Jun Zhang, Pei Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
9.3field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

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  12. Nobiletin-mediated autophagy mitigates nanoplastic-induced toxicity in human intestinal Caco-2 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

5 authors at 4 institutions in 1 country.

Haidong WangDepartment of Pharmacy, The Affiliated Lianyungang Hospital of Xuzhou Medical University/The First People's Hospital of Lianyungang, Lianyungang, 222000, People's Republic of China.
Yujin GuoAffiliated Jining First People's Hospital of Jining Medical University, Jining Medical University, No. 6, Jiankang Road, Jining, 272000, Shandong, People's Republic of China.
Yi QiaoDepartment of Public Health, Jining Medical University, Jining, 272000, People's Republic of China.
Jun ZhangDepartment of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
Pei JiangAffiliated Jining First People's Hospital of Jining Medical University, Jining Medical University, No. 6, Jiankang Road, Jining, 272000, Shandong, People's Republic of China. jiangpeicsu@sina.com.ORCID http://orcid.org/0000-0001-8790-5643
Jining First People's Hospital · CNFirst Affiliated Hospital of Zhengzhou University · CNJining Medical University · CNXuzhou Medical College · CN

Funding

National Natural Science Foundation of China (CN) 81602846
6 · The paper itself

Abstract

Multiple lines of evidence have shown that neuroinflammation and autophagy are highly involved in the process of depression. Nobiletin (NOB) displays neuroprotective effects and anti-depressant-like effects. Given the evidence that NOB exerts anti-inflammatory effects and regulates autophagy, we investigate the anti-neuroinflammatory properties and the effect of regulating the autophagy of NOB and subsequently uncover the potential anti-depressant mechanisms of NOB. The behavioral changes of rats were observed after prolonged lipopolysaccharide (LPS) treatment and NOB administration. Rat hippocampus and BV2 cells treated by LPS and NOB were evaluated. The methods of real-time PCR analysis, Western blot, immunostaining, and adenovirus transfection were employed to determine neuroinflammation, autophagic markers, and nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) activation. Our study showed LPS enhanced the expression of pro-inflammatory cytokines and NLRP3 inflammasome activation but inhibited autophagy in both rat hippocampus and BV2 cells. NOB significantly improved the behavioral deficits and ameliorated the neuroinflammation induced by LPS in rats. Furthermore, NOB promoted autophagy and attenuated NLRP3 inflammasome activation induced by LPS, involving in the process the adenosine monophosphate-activated protein kinase (AMPK) pathway. Neuroprotective and anti-depressant actions of NOB relied on its effects of promoting autophagy and suppressing the activation of NLRP3, in which process of AMPK pathway may be involved.

Indexed as

AutophagySignal TransductionAMP-Activated Protein KinasesAnimalsBehavior, AnimalBrainCell LineFlavonesInflammasomesInflammationLipopolysaccharidesMaleMiceNLR Family, Pyrin Domain-Containing 3 ProteinRats, Sprague-DawleyAMP-Activated Protein KinasesFlavonesInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinnobiletinAMPKAutophagyDepressionNLRP3Nobiletin

Identifiers

PMID32833187
OpenAlexW3080481237

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.