Evidence map›Paper›PMID 24803746›Full record

ArticleMediators of inflammation2014

BHBA suppresses LPS-induced inflammation in BV-2 cells by inhibiting NF-κB activation.

Shou-Peng Fu, Su-Nan Li, Jian-Fa Wang, Yang Li, Shan-Shan Xie, Wen-Jing Xue, Hong-Mei Liu, Bing-Xu Huang, Qing-Kang Lv, Lian-Cheng Lei and 3 more

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 8% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

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21 more citing papers are in PubMed but not listed here.

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

13 authors at 1 institution in 1 country.

Shou-Peng FuCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Su-Nan LiCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Jian-Fa WangCollege of Veterinary Medicine, Jilin University, Changchun 130062, China ; College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing 163319, China.
Yang LiCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Shan-Shan XieCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Wen-Jing XueCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Hong-Mei LiuCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Bing-Xu HuangCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Qing-Kang LvCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Lian-Cheng LeiCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Guo-Wen LiuCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Wei WangCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Ju-Xiong LiuCollege of Veterinary Medicine, Jilin University, Changchun 130062, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Hydroxybutyric acid (BHBA) has neuroprotective effects, but the underlying molecular mechanisms are unclear. Microglial activation plays an important role in neurodegenerative diseases by producing several proinflammatory enzymes and proinflammatory cytokines. The current study investigates the potential mechanisms whereby BHBA affects the expression of potentially proinflammatory proteins by cultured murine microglial BV-2 cells stimulated with lipopolysaccharide (LPS). The results showed that BHBA significantly reduced LPS-induced protein and mRNA expression levels of iNOS, COX-2, TNF-α, IL-1β, and IL-6. Blocking of GPR109A by PTX resulted in a loss of this anti-inflammatory effect in BV-2 cells. Western blot analysis showed that BHBA reduced LPS-induced degradation of IκB-α and translocation of NF-κB, while no effect was observed on MAPKs phosphorylation. All results imply that BHBA significantly reduces levels of proinflammatory enzymes and proinflammatory cytokines by inhibition of the NF-κB signaling pathway but not MAPKs pathways, and GPR109A is essential to this function. Overall, these data suggest that BHBA has a potential as neuroprotective drug candidate in neurodegenerative diseases.

Indexed as

3-Hydroxybutyric AcidAnimalsCell LineI-kappa B ProteinsInflammationLipopolysaccharidesMiceNF-kappa BNF-KappaB Inhibitor alphaSignal Transduction3-Hydroxybutyric AcidI-kappa B ProteinsLipopolysaccharidesNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouse

Identifiers

PMID24803746
PMCPMC3997897
OpenAlexW2083625027

What OpenQuestion holds

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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.