Evidence map›Paper›PMID 25322283›Full record

ArticleMolecules (Basel, Switzerland)2014

Anti-inflammatory potential of newly synthesized 4-[(butylsulfinyl)methyl]-1,2-benzenediol in lipopolysaccharide-stimulated BV2 microglia.

Guk-Heui Jo, Il-Whan Choi, Jin-Woo Jeong, Gi-Young Kim, Jinwoo Kim, Hongsuk Suh, Chung-Ho Ryu, Wun-Jae Kim, Yung Hyun 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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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 6 institutions in 1 country.

Guk-Heui JoDepartment of Biochemistry, College of Korean Medicine, Dongeui University, Busan 614-052, Korea. cooki28@naver.com.
Il-Whan ChoiDepartment of Microbiology, College of Medicine, Inje University, Busan 608-756, Korea. cihima@inje.ac.kr.
Jin-Woo JeongDivision of Applied Life Science (BK21 Plus), Gyeongsang National University, Jinju 660-701, Korea. immune-jeong@gnu.ac.kr.
Gi-Young KimDepartment of Marine Life Sciences, Jeju National University, Jeju 690-756, Korea. immunkim@cheju.ac.kr.
Jinwoo KimDepartment of Chemistry and Chemistry Institute for Functional Materials, Pusan National University, Busan 609-735, Korea. jinwoo@pusan.ac.kr.
Hongsuk SuhDepartment of Chemistry and Chemistry Institute for Functional Materials, Pusan National University, Busan 609-735, Korea. hssuh@pusan.ac.kr.
Chung-Ho RyuDivision of Applied Life Science, Gyeongsang National University, Jinju 660-701, Korea. ryu@gnu.ac.kr.
Wun-Jae KimDepartment of Urology, College of Medicine, Chungbuk National University, Cheongju 361-763, Korea. wjkim@chungbuk.ac.kr.
Yung Hyun ChoiDepartment of Biochemistry, College of Korean Medicine, Dongeui University, Busan 614-052, Korea. choiyh@deu.ac.kr.
Dong-Eui University · KRGyeongsang National University · KRPusan National University · KRChungbuk National University · KRInje University · KRJeju National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we investigated the anti-inflammatory effects of newly synthesized 4-[(butylsulfinyl)methyl]-1,2-benzenediol (SMBD) in lipopolysaccharide (LPS)-stimulated BV2 microglia and the subsequent signaling events. Following stimulation with LPS, elevated production of nitric oxide (NO) and prostaglandin E2 (PGE2) was detected in BV2 cells; however, SMBD pretreatment inhibited the production of NO and PGE2 through suppressing gene expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), respectively, at non-toxic concentrations. LPS-stimulated gene expression and production of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were also significantly reduced by SMBD. The anti-inflammatory effects of SMBD were associated with suppression of LPS-induced nuclear translocation of nuclear factor-kappa B (NF-κB), and phosphorylation of mitogen-activated protein kinases (MAPKs) and Akt, a phosphatidylinositol 3-kinase (PI3K) downstream effector. Therefore, the present results demonstrate that SMBD down-regulates inflammatory gene expression by inhibiting the activation of NF-κB through interference with the activation of MAPKs and PI3K/Akt signaling. Taken together, our data suggest that SMBD may have potential to be developed into an effective anti-inflammatory agent.

Indexed as

AnimalsAnti-Inflammatory AgentsCatecholsCell LineCell SurvivalCyclooxygenase 2CytokinesDinoprostoneGene Expression RegulationLipopolysaccharidesMiceMicrogliaNitric Oxide Synthase Type IIOxidoreductasesSignal TransductionSulfoxides4-((butylsulfinyl)methyl)-1,2-benzenediolAnti-Inflammatory AgentscatecholCatecholsCyclooxygenase 2CytokinesDinoprostoneLipopolysaccharidesnitric-oxide reductaseNitric Oxide Synthase Type IINos2 protein, mouseOxidoreductasesPtgs2 protein, mouseSulfoxides

Identifiers

PMID25322283
PMCPMC6270807
OpenAlexW1971081661

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.