Evidence map›Paper›PMID 28217098›Full record

ArticleFrontiers in pharmacology2017

Quercetin Inhibits LPS-Induced Inflammation and ox-LDL-Induced Lipid Deposition.

Feng Xue, Xiaobo Nie, Jianping Shi, Qingxue Liu, Ziwei Wang, Xiting Li, Jinqiu Zhou, Jia Su, Mingming Xue, Wei-Dong Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 79 citations in OpenAlex.

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  11. Immune cell-mediated features of atherosclerosis.Frontiers in cardiovascular medicine · 2024
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  15. Key ingredients inFrontiers in plant science · 2023
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  20. PARP-1-Associated Pathological Processes: Inhibition by Natural Polyphenols.International journal of molecular sciences · 2021
    Review
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

11 authors at 3 institutions in 1 country.

Feng XueKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University Hohhot, China.
Xiaobo NieKey Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University Kaifeng, China.
Jianping ShiChinese Internal Medicine Teaching and Researching Section, Inner Mongolia Medical University Hohhot, China.
Qingxue LiuKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University Hohhot, China.
Ziwei WangState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Xiting LiKey Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University Kaifeng, China.
Jinqiu ZhouInternal Medicine Section, No. 253 Hospital of PLA Hohhot, China.
Jia SuState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Mingming XueKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University Hohhot, China.
Wei-Dong ChenKey Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical UniversityHohhot, China; Key Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan UniversityKaifeng, China.
Yan-Dong WangState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Inner Mongolia Medical University · CNBeijing University of Chemical Technology · CNHenan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant activation of inflammation and excess accumulation of lipids play crucial role in the occurrence and progression of atherosclerosis (AS). Quercetin (QCT) has been tested effectively to cure AS. It is widely distributed in plant foods and has been proved to have potential antioxidative and anticancer activities. However, the underlying molecular mechanisms of OCT in AS are not completely understood. In the present study, we stimulated murine RAW264.7 cells with lipopolysaccharide (LPS) or oxidized low-density lipoproteins (ox-LDL) to mimic the development of AS. The data show that QCT treatment leads to an obvious decrease of multiple inflammatory cytokines in transcript level, including interleukin (IL)-1α, IL-1β, IL-2, IL-10, macrophage chemoattractant protein-1 (MCP-1), and cyclooxygenase-2 (COX-2) induced by LPS. Moreover, expressions of other factors that contribute to the AS development, such as matrix metalloproteinase-1 (MMP-1) and suppressor of cytokine signaling 3 (SOCS3) induced by LPS are also downregulated by QCT. Furthermore, we found that QCT suppressed LPS-induced the phosphorylation of STAT3. Meanwhile, QCT could ameliorate lipid deposition and overproduction of reactive oxygen species induced by ox-LDL, and block the expression of lectin-like oxidized LDL receptor-1 (LOX-1) in cultured macrophages. Taken together, our data reveal that QCT has obvious anti-inflammatory and antioxidant virtues and could be a therapeutic agent for the prevention and treatment of AS.

Indexed as

atherosclerosis (AS)inflammationlipid depositionMongolian medicinequercetin (QCT)

Identifiers

PMID28217098
PMCPMC5289956
OpenAlexW2584573426

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.