Evidence map›Paper›PMID 28732502›Full record

ArticleJournal of neuroinflammation2017

Chronic glucocorticoid exposure activates BK-NLRP1 signal involving in hippocampal neuron damage.

Biqiong Zhang, Yaodong Zhang, Wenning Wu, Tanzhen Xu, Yanyan Yin, Junyan Zhang, Dake Huang, Weizu Li

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 71 citations in OpenAlex.

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  16. Key Mechanisms and Potential Implications ofAntioxidants (Basel, Switzerland) · 2021
    Article
  17. BK Channels Regulate LPS-induced CCL-2 Release from Human Pulmonary Endothelial Cells.American journal of respiratory cell and molecular biology · 2021
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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 1 institution in 1 country.

Biqiong ZhangDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Yaodong ZhangDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Wenning WuDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Tanzhen XuDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Yanyan YinDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Junyan ZhangDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Dake HuangDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Weizu LiDepartment of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China. liweizu@126.com.ORCID 0000-0002-8305-1414
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation mediated by NLRP1 (nucleotide-binding oligomerization domain (NOD)-like receptor protein 1) inflammasome plays an important role in many neurological diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD). Our previous studies showed that chronic glucocorticoid (GC) exposure increased brain inflammation via NLRP1 inflammasome and induce neurodegeneration. However, little is known about the mechanism of chronic GC exposure on NLRP1 inflammasome activation in hippocampal neurons.

methodsHippocampal neurons damage was assessed by LDH kit and Hoechst 33258 staining. The expression of microtubule-associated protein 2 (MAP2), inflammasome complex protein (NLRP1, ASC and caspase-1), inflammatory cytokines (IL-1β), and large-conductance Ca

resultsChronic dexamethasone (DEX) treatment significantly increased LDH release and neuronal apoptosis and decreased expression of MAP2. The mechanistic studies revealed that chronic DEX exposure significantly increased the expression of NLRP1, ASC, caspase-1, IL-1β, L-18, and BK protein and NLRP1, IL-1β and BK mRNA levels in hippocampal neurons. Further studies showed that DEX exposure results in the increase of BK channel currents, with the subsequent K

conclusionOur findings suggest that chronic GC exposure may increase neuroinflammation via activation of BK-NLRP1 signal pathway and promote hippocampal neurons damage, which may be involved in the development and progression of AD.

Indexed as

HippocampusAnimalsAnimals, NewbornApoptosisBrain InjuriesCells, CulturedDexamethasoneDisease Models, AnimalGlucocorticoidsL-Lactate DehydrogenaseMembrane PotentialsMiceMice, Inbred ICRMicrotubule-Associated ProteinsNerve Tissue ProteinsNeuronsDexamethasoneGlucocorticoidsiberiotoxinL-Lactate DehydrogenaseMAP2 protein, ratMicrotubule-Associated ProteinsNerve Tissue ProteinsNlrp1a protein, ratPeptidesSynaptotagminsSyt17 protein, ratAlzheimer’s diseaseBK channelsGlucocorticoidsNeuroinflammationNLRP1 inflammasome

Identifiers

PMID28732502
PMCPMC5521122
OpenAlexW2737201549

What OpenQuestion holds

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LicenceCC BY
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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.