Evidence map›Paper›PMID 28420166›Full record

ArticleInternational journal of molecular sciences2017

Hypaphorine Attenuates Lipopolysaccharide-Induced Endothelial Inflammation via Regulation of TLR4 and PPAR-γ Dependent on PI3K/Akt/mTOR Signal Pathway.

Haijian Sun, Xuexue Zhu, Weiwei Cai, Liying Qiu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 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

4 authors at 1 institution in 1 country.

Haijian SunDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. haijsunjiangnan@jiangnan.edu.cn.
Xuexue ZhuDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. baojiangexz@sina.com.
Weiwei CaiDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. hlxuzhou11@sina.com.
Liying QiuDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. qiulydoc@163.com.
Jiangnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial lesion response to injurious stimuli is a necessary step for initiating inflammatory cascades in blood vessels. Hypaphorine (Hy) from different marine sources is shown to exhibit anti-inflammatory properties. However, the potential roles and possible molecular mechanisms of Hy in endothelial inflammation have yet to be fully clarified. We showed that Hy significantly inhibited the positive effects of lipopolysaccharide (LPS) on pro-inflammatory cytokines expressions, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and vascular cellular adhesion molecule-1 (VCAM-1), as well as induction of the phosphorylation of Akt and mTOR in HMEC-1 cells. The downregulated peroxisome proliferator-activated receptor γ (PPAR-γ) and upregulated toll-like receptor 4 (TLR4) expressions in LPS-challenged endothelial cells were prevented by Hy. Inhibition of both PI3K and mTOR reversed LPS-stimulated increases in TLR4 expressions and decreases in PPAR-γ levels. Genetic silencing of TLR4 or PPAR-γ agonist pioglitazone obviously abrogated the levels of pro-inflammatory cytokines in LPS-treated HMEC-1 cells. These results suggest that Hy may exert anti-inflammatory actions through the regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathways. Hy may be considered as a therapeutic agent that can potentially relieve or ameliorate endothelial inflammation-associated diseases.

Indexed as

BiomarkersCytokinesEndothelium, VascularEnzyme ActivationHumansIndolesInflammationInflammation MediatorsLipopolysaccharidesPhosphatidylinositol 3-KinasesPPAR gammaProtein BindingProto-Oncogene Proteins c-aktSignal TransductionToll-Like Receptor 4TOR Serine-Threonine KinasesBiomarkersCytokinesIndolesInflammation MediatorslenticinLipopolysaccharidesPhosphatidylinositol 3-KinasesPPAR gammaProto-Oncogene Proteins c-aktToll-Like Receptor 4TOR Serine-Threonine Kinasesendothelial cellsinflammationLPSPPAR-γTLR4

Identifiers

PMID28420166
PMCPMC5412428
OpenAlexW2605825283

What OpenQuestion holds

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LicenceCC BY
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.