Evidence map›Paper›PMID 32210361›Full record

ArticleThe Journal of antibiotics2020

Inhibition of cellular inflammatory mediator production and amelioration of learning deficit in flies by deep sea Aspergillus-derived cyclopenin.

Liyan Wang, Mengjie Li, Yinzhi Lin, Shuwen Du, Zhenyu Liu, Jianhua Ju, Hiromi Suzuki, Makoto Sawada, Kazuo Umezawa

Abstract read
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In one paragraph

Article in The Journal of antibiotics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-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

13 citing papers in PubMed, 23 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 4 institutions in 2 countries.

Liyan WangCollege of Life Sciences and Oceanography, Shenzhen Key Laboratory of Marine Bio-resource and Eco-environmental Science, Shenzhen University, 518060, Shenzhen, China.
Mengjie LiCollege of Life Sciences and Oceanography, Shenzhen Key Laboratory of Marine Bio-resource and Eco-environmental Science, Shenzhen University, 518060, Shenzhen, China.
Yinzhi LinDepartment of Molecular Target Medicine, Aichi Medical University School of Medicine, 480-1195, Nagakute, Japan.
Shuwen DuBeijing JoeKai Biotech LLC, 10094, Beijing, China.
Zhenyu LiuBeijing JoeKai Biotech LLC, 10094, Beijing, China.
Jianhua JuCAS Key Laboratory of Tropical Marine Bio-resources and Ecology, RNAM Center for Marine Microbiology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, 510301, Guangdong, China.ORCID http://orcid.org/0000-0001-7712-8027
Hiromi SuzukiBrain Functions, Research Institute of Environmental Medicine, Nagoya University, 464-8601, Nagoya, Japan.
Makoto SawadaBrain Functions, Research Institute of Environmental Medicine, Nagoya University, 464-8601, Nagoya, Japan.
Kazuo UmezawaDepartment of Molecular Target Medicine, Aichi Medical University School of Medicine, 480-1195, Nagakute, Japan. umezawa@aichi-med-u.ac.jp.
Aichi Medical University · JPNagoya University · JPShenzhen University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the course of screening lipopolysaccharide (LPS)-induced nitric oxide (NO) production inhibitors, two related benzodiazepine derivatives, cyclopenol and cyclopenin, were isolated from the extract of a deep marine-derived fungal strain, Aspergillus sp. SCSIOW2. Cyclopenol and cyclopenin inhibited the LPS-induced formation of NO and secretion of IL-6 in RAW264.7 cells at nontoxic concentrations. In terms of the mechanism underlying these effects, cyclopenol and cyclopenin were found to inhibit the upstream signal of NF-κB activation. These compounds also inhibited the expression of IL-1β, IL-6, and inducible nitric oxide synthase (iNOS) in mouse microglia cells, macrophages in the brain. In relation to the cause of Alzheimer's disease, amyloid-β-peptide is known to induce inflammation in the brain. Therefore, the present study investigated the ameliorative effects of these inhibitors on an in vivo Alzheimer's model using flies. Learning deficits were induced by the overexpression of amyloid-β42 in flies, and cyclopenin but not cyclopenol was found to rescue learning impairment. Therefore, novel anti-inflammatory activities of cyclopenin were identified, which may be useful as a candidate of anti-inflammatory agents for neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnimalsAnti-Inflammatory AgentsAspergillusBenzodiazepinonesCell LineDipteraDisease Models, AnimalInflammationInterleukin-1betaLearning DisabilitiesLipopolysaccharidesMacrophagesMiceMicrogliaNF-kappa BAnti-Inflammatory AgentsBenzodiazepinonescyclopenincyclopenolInterleukin-1betaLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type II

Identifiers

PMID32210361
OpenAlexW3012713076

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.