Evidence map›Paper›PMID 30470771›Full record

ArticleScientific reports2018

On the use of abiotic sialic acids to attenuate cell inflammation.

Zhongwei Xue, Hu Zhao, Rui Zhu, Congcong Chen, Hongzhi Cao, Jiahuai Han, Shoufa Han

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. An In Vitro Model to Investigate the Role ofInternational journal of molecular sciences · 2020
    Article
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

7 authors at 2 institutions in 1 country.

Zhongwei XueDepartment of Chemical Biology, College of Chemistry and Chemical Engineering, State Key Laboratory for Physical Chemistry of Solid Surfaces, the Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China.
Hu ZhaoDepartment of Chemical Biology, College of Chemistry and Chemical Engineering, State Key Laboratory for Physical Chemistry of Solid Surfaces, the Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China.
Rui ZhuDepartment of Chemical Biology, College of Chemistry and Chemical Engineering, State Key Laboratory for Physical Chemistry of Solid Surfaces, the Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China.
Congcong ChenNational Glycoengineering research center, Shandong University, Jinan, 250012, China.
Hongzhi CaoNational Glycoengineering research center, Shandong University, Jinan, 250012, China.ORCID http://orcid.org/0000-0003-4736-3143
Jiahuai HanState key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361005, China.
Shoufa HanDepartment of Chemical Biology, College of Chemistry and Chemical Engineering, State Key Laboratory for Physical Chemistry of Solid Surfaces, the Key Laboratory for Chemical Biology of Fujian Province, The MOE Key Laboratory of Spectrochemical Analysis & Instrumentation, and Innovation Center for Cell Biology, Xiamen University, Xiamen, 361005, China. shoufa@xmu.edu.cn.ORCID http://orcid.org/0000-0002-2057-0559
Xiamen University · CNShandong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 21572189National Natural Science Foundation of China (National Science Foundation of China) 21775130
6 · The paper itself

Abstract

Sialic acid (Sia) residues on cell surface are critical for myriad cellular events such as immunity and inflammation. We herein reported the use of abiotic Sia to raise the thresholds of inflammatory cell responses. Identified from a panel of structurally diversified Sia analogs via a cell inflammation assay, Sia-2, with N-butyryl moiety at C-5, markedly lowered LPS-stimulated NF-κB activity in macrophages. Further analysis shows that Sia-2 attenuates phosphorylation of IκB and Erk1/2/p38/JNK, critical for NF-κB signaling and MAPK signaling, and lowers gene transcription of proinflammatory interleukin-6. These results support the use of abiotic Sia as promising agents to modulate cell surface Sia-pertinent cell signaling.

Indexed as

AnimalsAnti-Inflammatory AgentsGene Expression RegulationInflammationInterleukin-6MacrophagesMiceMitogen-Activated Protein KinasesNF-kappa BPhosphorylationRAW 264.7 CellsSialic AcidsSignal TransductionStress, PhysiologicalAnti-Inflammatory AgentsInterleukin-6interleukin-6, mouseMitogen-Activated Protein KinasesNF-kappa BSialic Acids

Identifiers

PMID30470771
PMCPMC6251910
OpenAlexW2900501672

What Socratic 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 Socratic graph.