Evidence map›Paper›PMID 25047101›Full record

ArticleInflammation2015

MAPK and NF-κB pathways are involved in bisphenol A-induced TNF-α and IL-6 production in BV2 microglial cells.

Jingying Zhu, Lei Jiang, Yanqing Liu, Wenyi Qian, Jingli Liu, Jing Zhou, Rong Gao, Hang Xiao, Jun Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 116 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 2 institutions in 1 country.

Jingying ZhuKey Lab of Modern Toxicology (NJMU), Ministry of Education. Department of Toxicology, School of Public Health, Nanjing Medical University, 818 Tianyuan East Road, Nanjing, Jiangsu, 211166, China.
Lei Jiang
Yanqing Liu
Wenyi Qian
Jingli Liu
Jing Zhou
Rong Gao
Hang Xiao
Jun Wang
Nanjing Medical University · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial activation has been reported to play an important role in neurodegenerative diseases by producing pro-inflammatory cytokines. Bisphenol A (BPA, 2,2-bis (4-hydroxyphenyl) propane), known as a ubiquitous endocrine-disrupting chemical, is reported to perform both mimic- and anti-estrogen properties; however, whether it affects cytokine production or immune response in central nervous system remains unclear. The present study was aimed to explore whether BPA was involved in inflammatory action and to investigate the potential mechanisms in microglial cells. BV2, the murine microglial cell line, was used in the present work as the cell model. BPA-associated morphologic changes, cytokine responses, and signaling events were examined using immunofluorescence analysis, real-time PCR, enzyme-linked immunosorbent assay, and western blot. Our results indicated that BPA increased BV2 cells activation and simultaneously elevated tumor necrosis factor-α and interleukin 6 expression, which could be partially reversed by estrogen receptor antagonist, ICI182780. In addition, the c-Jun N-terminal protein kinase (JNK) inhibitor (SP600125), rather than ERK1/2 blocker (PD98059), displayed anti-inflammatory properties on BPA-elicited cytokine responses. Moreover, the inflammatory transcription factor NF-κB was specifically activated by BPA as well. These results, taken together, suggested that BPA may have functional effects on the response of microglial cell activation via, in part, the estrogen receptor, JNK, ERK mitogen-activated protein kinase, and NF-κB signaling pathways with its subsequent influence on pro-inflammatory action.

Indexed as

AnimalsAnthracenesAnti-Inflammatory AgentsBenzhydryl CompoundsBisphenol A CompoundsCell LineEndocrine DisruptorsEnzyme ActivationEstradiolEstrogen Receptor AntagonistsEstrogen Receptor ModulatorsEstrogensExtracellular Signal-Regulated MAP KinasesFlavonoidsFulvestrantInflammation2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAnthracenesAnti-Inflammatory AgentsBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEndocrine DisruptorsEstradiolEstrogen Receptor AntagonistsEstrogen Receptor ModulatorsEstrogensExtracellular Signal-Regulated MAP KinasesFlavonoidsFulvestrantInterleukin-6JNK Mitogen-Activated Protein KinasesNF-kappa BPhenolspyrazolanthroneTumor Necrosis Factor-alpha

Identifiers

PMID25047101
OpenAlexW2081058440

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.