Evidence map›Paper›PMID 25429561›Full record

ArticleMolecules (Basel, Switzerland)2014

EOP, a newly synthesized ethyl pyruvate derivative, attenuates the production of inflammatory mediators via p38, ERK and NF-κB pathways in lipopolysaccharide-activated BV-2 microglial cells.

Soon Min, Sandeep Vasant More, Ju-Young Park, Sae-Bom Jeon, Shin Young Park, Eun-Jung Park, Sung-Hwa Yoon, Dong-Kug Choi

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 18 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

8 authors at 3 institutions in 1 country.

Soon MinDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea.
Sandeep Vasant MoreDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea.
Ju-Young ParkDepartment of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea.
Sae-Bom JeonBranch of Immune and Cell Therapy, National Cancer Center, Goyang 410-769, Korea.
Shin Young ParkDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea.
Eun-Jung ParkBranch of Immune and Cell Therapy, National Cancer Center, Goyang 410-769, Korea.
Sung-Hwa YoonDepartment of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea.
Dong-Kug ChoiDepartment of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea. choidk@kku.ac.kr.
Konkuk University · KRAjou University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia-induced neuroinflammation is an important pathological mechanism influencing various neurodegenerative disorders. Excess activation of microglia produces a myriad of proinflammatory mediators that decimate neurons. Hence, therapeutic strategies aimed to suppress the activation of microglia might lead to advancements in the treatment of neurodegenerative diseases. In this study, we synthesized a novel ethyl pyruvate derivative, named EOP (S-ethyl 2-oxopropanethioate) and studied its effects on lipopolysaccharide (LPS)-induced production of nitric oxide (NO) in rat primary microglia and mouse BV-2 microglia. EOP significantly decreased the production of NO, inducible nitric oxide synthase, cyclooxygenase and other proinflammatory cytokines, such as interleukin (IL)-6, IL-1β and tumor necrosis factor-α, in LPS-stimulated BV-2 microglia. The phosphorylation levels of extracellular regulated kinase, p38 mitogen-activated protein kinase, and nuclear translocation of NF-κB were also inhibited by EOP in LPS-activated BV-2 microglial cells. Overall, our observations indicate that EOP might be a promising therapeutic agent to diminish the development of neurodegenerative diseases associated with microglia activation.

Indexed as

AnimalsCell DeathCell LineCell SurvivalCyclooxygenase 2CytokinesExtracellular Signal-Regulated MAP KinasesI-kappa B ProteinsInflammation MediatorsLipopolysaccharidesMiceMicrogliaNF-kappa BNF-KappaB Inhibitor alphaNitric OxideNitric Oxide Synthase Type IICyclooxygenase 2Cytokinesethyl pyruvateExtracellular Signal-Regulated MAP KinasesI-kappa B ProteinsInflammation MediatorsLipopolysaccharidesNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouseNfkbia protein, ratNitric OxideNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesPyruvatesS-ethyl 2-oxopropanethioate

Identifiers

PMID25429561
PMCPMC6271075
OpenAlexW2069846335

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.