Evidence map›Paper›PMID 34817756›Full record

ArticleMetabolic brain disease2022

Neuroprotective effects of liraglutide against inflammation through the AMPK/NF-κB pathway in a mouse model of Parkinson's disease.

Bing Cao, Yanqiu Zhang, Jinhu Chen, Pengyue Wu, Yuxuan Dong, Yanqin Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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  13. GLP-1 Receptor Agonists: A New Treatment in Parkinson's Disease.International journal of molecular sciences · 2024
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  18. Neuroprotective effect of engineeredBioengineering & translational medicine · 2023
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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.

Bing CaoDepartment of Physiology, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei, 050024, People's Republic of China.
Yanqiu ZhangDepartment of Physiology, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei, 050024, People's Republic of China.
Jinhu ChenDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, 050051, People's Republic of China.
Pengyue WuDepartment of Physiology, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei, 050024, People's Republic of China.
Yuxuan DongDepartment of Physiology, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei, 050024, People's Republic of China.
Yanqin WangDepartment of Physiology, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei, 050024, People's Republic of China. yqw1016@163.com.ORCID http://orcid.org/0000-0001-5056-1963
Hebei Normal University · CNHebei General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disease with increasing incidence in aged populations, second only to Alzheimer's disease. Increasing evidence has shown that inflammation plays an important role in the occurrence and development of Parkinson's disease. Growing evidence has shown that AMP-activated protein kinase (AMPK) and NF-κB are closely related to inflammation. Glucagon-like peptide 1 (GLP-1) is a hormone that is primarily secreted by intestinal endocrine L cells, and it has a variety of physiology through binding to GLP-1 receptor. GLP-1can be used for treatment of type 2 diabetes. In addition, GLP-1 also has anti-neuroinflammation activity. However, the exact mechanism behind how GLP-1 regulates neuroinflammation remains unclear. This study was designed to examine the effect of liraglutide on 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP)-induced injury in mice and its potential mechanism of action. Results showed that liraglutide dose-dependently ameliorated mouse behavior including swimming time and locomotor activity, increased the number of tyrosine hydroxylase (TH)-positive neurons and protein level, and reduced Iba1 and GFAP expression in the substantia nigra (SN). Liraglutide treatment also increased p-AMPK expression and reduced NF-κB protein level. Applying the AMPK inhibitor Dorsomorphin (Compound C) reversed the effect of liraglutide-reducing p-AMPK and increasing NF-κB expression. Finally, GFAP protein level increased, along with a decrease in TH expression. In conclusion, these results suggest that liraglutide can suppress neuroinflammation. Moreover, this effect is mediated through the AMPK/NF-κB signaling pathway.

Indexed as

Diabetes Mellitus, Type 2Neurodegenerative DiseasesNeuroprotective AgentsParkinson DiseaseAMP-Activated Protein KinasesAnimalsDisease Models, AnimalInflammationLiraglutideMiceNF-kappa BAMP-Activated Protein KinasesLiraglutideNeuroprotective AgentsNF-kappa BAMPKLiraglutideNeuroinflammationNF-κBParkinson’s disease

Identifiers

PMID34817756
OpenAlexW3215934804

What OpenQuestion holds

Texttitle and abstract
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.