Evidence map›Paper›PMID 30327995›Full record

ArticleNeurochemical research2018

A Novel and Selective p38 Mitogen-Activated Protein Kinase Inhibitor Attenuates LPS-Induced Neuroinflammation in BV2 Microglia and a Mouse Model.

Min Sung Gee, Sang-Won Kim, Namkwon Kim, Soo Jin Lee, Myung Sook Oh, Hee Kyung Jin, Jae-Sung Bae, Kyung-Soo Inn, Nam-Jung Kim, Jong Kil Lee

Abstract read
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In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 32 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

10 authors at 2 institutions in 1 country.

Min Sung GeeDepartment of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, South Korea.
Sang-Won KimDepartment of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, South Korea.
Namkwon KimDepartment of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul, South Korea.
Soo Jin LeeDepartment of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, South Korea.
Myung Sook OhDepartment of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul, South Korea.
Hee Kyung JinDepartment of Laboratory Animal Medicine, College of Veterinary Medicine, Kyungpook National University, Daegu, South Korea.
Jae-Sung BaeDepartment of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Kyung-Soo InnDepartment of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul, South Korea.
Nam-Jung KimDepartment of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, South Korea. kimnj@khu.ac.kr.
Jong Kil LeeDepartment of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, South Korea. jklee3984@khu.ac.kr.
Kyung Hee University · KRKyungpook National University · KR

Funding

National Research Foundation of Korea NRF-2016R1A2B4015169National Research Foundation of Korea NRF-2017R1A5A2014768
6 · The paper itself

Abstract

Neuroinflammation is an important pathological feature in neurodegenerative diseases. Accumulating evidence has suggested that neuroinflammation is mainly aggravated by activated microglia, which are macrophage like cells in the central nervous system. Therefore, the inhibition of microglial activation may be considered for treating neuroinflammatory diseases. p38 mitogen-activated protein kinase (MAPK) has been identified as a crucial enzyme with inflammatory roles in several immune cells, and its activation also relates to neuroinflammation. Considering the proinflammatory roles of p38 MAPK, its inhibitors can be potential therapeutic agents for neurodegenerative diseases relating to neuroinflammation initiated by microglia activation. This study was designed to evaluate whether NJK14047, a recently identified novel and selective p38 MAPK inhibitor, could modulate microglia-mediated neuroinflammation by utilizing lipopolysaccharide (LPS)-stimulated BV2 cells and an LPS-injected mice model. Our results showed that NJK14047 markedly reduced the production of nitric oxide and prostaglandin E

Indexed as

AnimalsCell LineDose-Response Relationship, DrugImidazolesInflammationInflammation MediatorsLipopolysaccharidesMaleMiceMice, Inbred C57BLMicrogliap38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsPyridinesImidazolesInflammation MediatorsLipopolysaccharidesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsPyridinesSB 203580Kinase inhibitorLipopolysaccharideMicrogliaNeuroinflammationP38 mitogen-activated protein kinase

Identifiers

PMID30327995
OpenAlexW2896026301

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.