Evidence map›Paper›PMID 29267220›Full record

ArticleInternational journal of molecular sciences2017

Galangin Reduces the Loss of Dopaminergic Neurons in an LPS-Evoked Model of Parkinson's Disease in Rats.

Guangxin Chen, Juxiong Liu, Liqiang Jiang, Xin Ran, Dewei He, Yuhang Li, Bingxu Huang, Wei Wang, Shoupeng Fu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
7.2field-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

31 citing papers in PubMed, 120 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

9 authors at 1 institution in 1 country.

Guangxin ChenCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. chengx15@mails.jlu.edu.cn.
Juxiong LiuCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. juxiong@jlu.edu.cn.
Liqiang JiangCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. jianglq9914@mails.jlu.edu.cn.
Xin RanCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. ranxin9914@mails.jlu.edu.cn.
Dewei HeCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. hedw9914@mails.jlu.edu.cn.
Yuhang LiCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. yhli9915@mails.jlu.edu.cn.
Bingxu HuangCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. huangbingxu16@mails.jlu.edu.cn.
Wei WangCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. wangwei@jlu.edu.cn.
Shoupeng FuCollege of Animal Science and Veterinary Medicine, Jilin University, Changchun 130062, China. fushoupeng@jlu.edu.cn.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is caused by the loss of dopaminergic (DA) neurons in the midbrain substantia nigra (SN). Neuroinflammation, which is marked by microglial activation, plays a very important role in the pathogenesis of PD. Pro-inflammatory mediators produced by activated microglia could damage DA neurons. Hence, the inhibition of microglial activation may provide a new approach for treating PD. Galangin has been shown to inhibit inflammation in a variety of diseases, but not PD. In this study, we aimed to investigate the anti-inflammatory effect of galangin and the underlying mechanisms in Lipopolysaccharide (LPS) induced PD models. We first examined the protective effect of galangin in the LPS-induced PD rat model. Specifically, we investigated the effects on motor dysfunction, microglial activation, and the loss of DA neurons. Then, galangin was used to detect the impact on the inflammatory responses and inflammatory signaling pathways in LPS-induced BV-2 cells. The in vivo results showed that galangin dose-dependently attenuates the activation of microglia, the loss of DA neurons, and motor dysfunction. In vitro, galangin markedly inhibited LPS-induced expression of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β), cyclooxygenase 2 (COX-2), and induced nitric oxide synthase (iNOS) via associating with the phosphorylation of c-JUN N-terminal Kinase (JNK), p38, protein kinase B (AKT), and nuclear factor κB (NF-κB) p65. Collectively, the results indicated that galangin has a role in protecting DA neurons by inhibiting microglial activation.

Indexed as

AnimalsAnti-Inflammatory AgentsBiomarkersCell LineCell SurvivalDisease Models, AnimalDopaminergic NeuronsDose-Response Relationship, DrugFlavonoidsInflammationLipopolysaccharidesMiceMicrogliaNeuroprotective AgentsParkinson DiseaseRatsAnti-Inflammatory AgentsBiomarkersFlavonoidsgalanginLipopolysaccharidesNeuroprotective AgentsAKTgalanginMAPKsmicrogliaNF-κBParkinson’s disease

Identifiers

PMID29267220
PMCPMC5795964
OpenAlexW2785178575

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.