Evidence map›Paper›PMID 31915845›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Dexamethasone sodium phosphate attenuates lipopolysaccharide-induced neuroinflammation in microglia BV2 cells.

Bin Hui, Xin Yao, Liping Zhang, Qinhua Zhou

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  6. Neuroprotective Effects of Dexamethasone in a Neuromelanin-Driven Parkinson's Disease Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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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

4 authors at 3 institutions in 1 country.

Bin HuiCollege of Pharmacy, Shanghai University of Medical & Health Sciences, Shanghai, China.
Xin YaoJiyuan Shi People's Hospital, Jiyuan, Henan, China.
Liping ZhangDepartment of Emergency Medicine, Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China. gszlp29@sina.com.
Qinhua ZhouCollege of Medicine, Jiaxing University, Jiaxing, China. zhouqh2016@aliyun.com.
Jiaxing University · CNShanghai Jiao Tong University · CNShanghai University of Medicine and Health Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal neuroinflammation ignited by overproduction of chemokines and cytokines via microglial cells can induce the occurrence and development of neurodegenerative disorders. The aim of this study is to investigate the effects of dexamethasone sodium phosphate (Dex-SP) on chemokine and cytokine secretion in lipopolysaccharide (LPS)-activated microglial cells. LPS markedly enhanced the secretion of pro-inflammatory factors such as regulated on activation, normal T cell expressed and secreted (RANTES), transforming growth factor beta-β1 (TGF-β1) and nitric oxide (NO), but decreased the production of macrophage inflammatory protein-1α (MIP-1α) and interleukin 10 (IL-10) in BV-2 microglial cells. Furthermore, LPS increased BV-2 microglial cell migration. However, Dex-SP treatment had the opposite effect, dampening the secretion of RANTES, TGF-β1, and NO, while increasing the production of MIP-1α and IL-10 and blocking migration of LPS-stimulated BV-2 microglial cells. Furthermore, Dex-SP markedly suppressed the LPS-induced degradation of IRAK-1 and IRAK-4, and blocked the activation in TRAF6, p-TAK1, and p-JNK in BV-2 microglial cells. These results showed that Dex-SP inhibited the neuroinflammatory response and migration in LPS-activated BV-2 microglia by inhibiting the secretion of RANTES, TGF-β1, and NO and increasing the production of MIP-1α and IL-10. The molecular mechanism of Dex-SP may be associated with inhibition of TRAF6/TAK-1/JNK signaling pathways mediated by IRAK-1 and IRAK-4.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineCell MovementCytokinesDexamethasoneInflammationInflammation MediatorsInterleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMicrogliaSignal TransductionAnti-Inflammatory AgentsCytokinesDexamethasonedexamethasone 21-phosphateInflammation MediatorsInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseIrak4 protein, mouseJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesTNF Receptor-Associated Factor 6TRAF6 protein, mouseChemokineCytokineDexamethasone sodium phosphateLPSMicroglia

Identifiers

PMID31915845
OpenAlexW2998939750

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.