Evidence map›Paper›PMID 29211014›Full record

ArticleInternational journal of molecular sciences2017

Lipopolysaccharide-Induced Nitric Oxide, Prostaglandin E2, and Cytokine Production of Mouse and Human Macrophages Are Suppressed by Pheophytin-b.

Chun-Yu Lin, Wen-Hung Wang, Shin-Huei Chen, Yu-Wei Chang, Ling-Chien Hung, Chung-Yi Chen, Yen-Hsu Chen

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 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

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  17. Equus β-Defensin-1 Regulates Innate IMMUNE Response inAnimals : an open access journal from MDPI · 2022
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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

7 authors at 3 institutions in 1 country.

Chun-Yu LinDivision of Infectious Diseases, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan. infectionman@gmail.com.
Wen-Hung WangDivision of Infectious Diseases, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan. bole0918@gmail.com.
Shin-Huei ChenSepsis Research Center, Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan. beautyhappy19@gmail.com.
Yu-Wei ChangSepsis Research Center, Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan. golden3p@gmail.com.
Ling-Chien HungDivision of Infectious Diseases, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan. lavender99kimo@yahoo.com.tw.
Chung-Yi ChenSchool of Medical and Health Sciences, Fooyin University, Kaohsiung 831, Taiwan. XX377@fy.edu.tw.ORCID 0000-0002-7026-3944
Yen-Hsu ChenDivision of Infectious Diseases, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan. infchen@gmail.com.ORCID 0000-0002-8667-4844
Kaohsiung Medical University · TWFooyin University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is an overwhelming systemic response to infection that frequently results in tissue damage, organ failure, and even death. Nitric oxide (NO), prostaglandin E2 (PGE2), and cytokine overproduction are thought to be associated with the immunostimulatory cascade in sepsis. In the present study, we analyzed the anti-inflammatory efficacy of the pheophytin-b on both RAW 264.7 murine macrophage and purified human CD14⁺ monocytes stimulated with lipopolysaccharide (LPS) and elucidated the mechanisms by analyzing the cell signaling pathways known to be activated in sepsis. Pheophytin-b suppressed the overexpression of NO, PGE2, and cytokines in LPS-stimulated macrophages without inducing cytotoxicity. It also reduced NOS2 and COX-2 mRNA and protein levels. The inhibitory effects on NO, PGE2, and cytokine overproduction arose from the suppression of STAT-1 and PI3K/Akt pathways; no changes in NF-κB, MAPK, and AP-1 signaling were detected. Thus, pheophytin-b may represent a potential candidate to beneficially modulate the inflammatory response in sepsis.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineCells, CulturedCytokinesDinoprostoneHumansLipopolysaccharidesMacrophagesMiceNitric OxidePheophytinsSignal TransductionAnti-Inflammatory AgentsCytokinesDinoprostoneLipopolysaccharidesNitric OxidePheophytinscytokinelipopolysaccharidemacrophagesnitric oxidepheophytin-bprostaglandin E2

Identifiers

PMID29211014
PMCPMC5751240
OpenAlexW2772906058

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.