Evidence map›Paper›PMID 27584788›Full record

ArticleCell death & disease2016

Kinsenoside screening with a microfluidic chip attenuates gouty arthritis through inactivating NF-κB signaling in macrophages and protecting endothelial cells.

Qiao Han, Wang Bing, Yin Di, Li Hua, Li Shi-He, Zheng Yu-Hua, Han Xiu-Guo, Wang Yu-Gang, Fan Qi-Ming, Yang Shih-Mo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

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  19. Targeting BRD4 prevents acute gouty arthritis by regulating pyroptosis.International journal of biological sciences · 2020
    Article
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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

11 authors at 6 institutions in 1 country.

Qiao HanShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Wang BingDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Yin DiComplex and Intelligent Research Center, School of Mechanical and Power Engineering, East China University of Science and Technology, Shanghai, People's Republic of China.
Li HuaDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Li Shi-HeDepartment of Orthopaedic Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, People's Republic of China.
Zheng Yu-HuaWenshan Zhengbao Orthopaedic Hospital of Yunnan Province, Wenshan, People's Republic of China.
Han Xiu-GuoShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Wang Yu-GangShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Fan Qi-MingShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Yang Shih-MoComplex and Intelligent Research Center, School of Mechanical and Power Engineering, East China University of Science and Technology, Shanghai, People's Republic of China.
Tang Ting-TingShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Shanghai Jiao Tong University · CNEast China University of Science and Technology · CNFirst Affiliated Hospital of Kunming Medical University · CNShanghai Ninth People's Hospital · CNKunming Medical University · CNPeople’s Hospital of Wenshan Prefecture · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gouty arthritis is a rheumatic disease that is characterized by the deposition of monosodium urate (MSU) in synovial joints cause by the increased serum hyperuricemia. This study used a three-dimensional (3D) flowing microfluidic chip to screen the effective candidate against MSU-stimulated human umbilical vein endothelial cell (HUVEC) damage, and found kinsenoside (Kin) to be the leading active component of Anoectochilus roxburghi, one of the Chinese medicinal plant widely used in the treatment of gouty arthritis clinically. Cell viability and apoptosis of HUVECs were evaluated, indicating that direct Kin stimulation and conditioned medium (CM) from Kin-treated macrophages both negatively modulated with MSU crystals. Additionally, Kin was capable of attenuating MSU-induced activation of nuclear factor-κB/mitogen-activated protein kinase (NF-κB/MAPK) signaling, targeting IκB kinase-α (IKKα) and IKKβ kinases of macrophages and influencing the expressions of NF-κB downstream cytokines and subsequent HUVEC bioactivity. Inflammasome NLR pyrin domain-containing 3 (NALP3) and toll-like receptor 2 (TLR2) were also inhibited after Kin treatment. Also, Kin downregulated CD14-mediated MSU crystals uptake in macrophages. In vivo study with MSU-injected ankle joints further revealed the significant suppression of inflammatory infiltration and endothelia impairment coupled with alleviation of ankle swelling and nociceptive response via Kin treatments. Taken together, these data implicated that Kin was the most effective candidate from Anoectochilus roxburghi to treat gouty arthritis clinically.

Indexed as

Drug Evaluation, Preclinical4-ButyrolactoneAnimalsAnti-Inflammatory AgentsArthritis, GoutyCrystallizationCulture Media, ConditionedCyclooxygenase 2CytokinesCytoprotectionExtremitiesHuman Umbilical Vein Endothelial CellsInflammasomesInflammation MediatorsLipopolysaccharide ReceptorsMacrophages3-glucopyranosyloxybutanolide4-ButyrolactoneAnti-Inflammatory AgentsCulture Media, ConditionedCyclooxygenase 2CytokinesInflammasomesInflammation MediatorsLipopolysaccharide ReceptorsMitogen-Activated Protein KinasesMonosaccharidesNF-kappa BUric Acid

Identifiers

PMID27584788
PMCPMC5059859
OpenAlexW2516630800

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.