Evidence map›Paper›PMID 29463000›Full record

ArticleInternational journal of molecular sciences2018

AWRK6, A Synthetic Cationic Peptide Derived from Antimicrobial Peptide Dybowskin-2CDYa, Inhibits Lipopolysaccharide-Induced Inflammatory Response.

Qiuyu Wang, Lili Jin, Huan Wang, Sijia Tai, Hongsheng Liu, Dianbao Zhang

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Anti-Inflammatory Activity of Peptides fromFoods (Basel, Switzerland) · 2024
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Inhibitory Effects of Antimicrobial Peptide JH-3 onMolecules (Basel, Switzerland) · 2019
    Article
  10. Article
  11. Article
  12. 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

6 authors.

Qiuyu WangSchool of Life Science, Liaoning University, Shenyang 110036, China. qiuyuwang@lnu.edu.cn.
Lili JinSchool of Life Science, Liaoning University, Shenyang 110036, China. lilijin@lnu.edu.cn.
Huan WangSchool of Life Science, Liaoning University, Shenyang 110036, China. wanghuan.lnu@gmail.com.
Sijia TaiSchool of Life Science, Liaoning University, Shenyang 110036, China. taisijia.lnu@gmail.com.
Hongsheng LiuResearch Center for Computer Simulating and Information Processing of Bio-macromolecules of Liaoning Province, Liaoning University, Shenyang 110036, China. liuhongsheng@lnu.edu.cn.
Dianbao ZhangDepartment of Stem Cells and Regenerative Medicine, Key Laboratory of Cell Biology, Ministry of Public Health of China, and Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, China. zhangdianbao@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipopolysaccharides (LPS) are major outer membrane components of Gram-negative bacteria and produce strong inflammatory responses in animals. Most antibiotics have shown little clinical anti-endotoxin activity while some antimicrobial peptides have proved to be effective in blocking LPS. Here, the anti-LPS activity of the synthetic peptide AWRK6, which is derived from antimicrobial peptide dybowskin-2CDYa, has been investigated in vitro and in vivo. The positively charged α-helical AWRK6 was found to be effective in blocking the binding of LBP (LPS binding protein) with LPS in vitro using ELISA. In a murine endotoxemia model, AWRK6 offered satisfactory protection efficiency against endotoxemia death, and the serum levels of LPS, IL-1β, IL-6, and TNF-α were found to be attenuated using ELISA. Further, histopathological analysis suggested that AWRK6 could improve the healing of liver and lung injury in endotoxemia mice. The results of real-time PCR and Western blotting showed that AWRK6 significantly reversed LPS-induced TLR4 overexpression and IκB depression, as well as the enhanced IκB phosphorylation. Additionally, AWRK6 did not produce any significant toxicity in vivo and in vitro. In summary, AWRK6 showed efficacious protection from LPS challenges in vivo and in vitro, by blocking LPS binding to LBP, without obvious toxicity, providing a promising strategy against LPS-induced inflammatory responses.

Indexed as

AnimalsAnti-Infective AgentsAntimicrobial Cationic PeptidesEndotoxemiaGene Expression RegulationGram-Negative BacteriaHumansInflammationInterleukin-1betaInterleukin-6LipopolysaccharidesMacrophagesMiceTumor Necrosis Factor-alphaAnti-Infective AgentsAntimicrobial Cationic PeptidesInterleukin-1betaInterleukin-6LipopolysaccharidesTumor Necrosis Factor-alphaantimicrobial peptideAWRK6inflammatory responselipopolysaccharides (LPS)

Identifiers

PMID29463000
PMCPMC5855822

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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.