Evidence map›Paper›PMID 32899525›Full record

ArticleMolecules (Basel, Switzerland)2020

Retrofractamide C Derived from

Hyung Jin Lim, Seon Gyeong Bak, Eun Jae Park, Sae-Kwang Ku, Soyoung Lee, Seung Woong Lee, Kang Min Lee, Seung-Jae Lee, Mun-Chual Rho

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. 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

9 authors at 3 institutions in 1 country.

Hyung Jin LimImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.
Seon Gyeong BakImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.
Eun Jae ParkImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.
Sae-Kwang KuDepartment of Anatomy and Histology, College of Korean Medicine, Daegu Haany University, Gyeongsan-si, Gyeonbuk 38610, Korea.ORCID 0000-0003-1269-3804
Soyoung LeeImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.
Seung Woong LeeImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.ORCID 0000-0003-1025-7363
Kang Min LeeDepartment of Molecular Biology, Chonbuk National University, Jeonju-si, Jeonbuk 54896, Korea.
Seung-Jae LeeImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.ORCID 0000-0002-1908-7666
Mun-Chual RhoImmunoregulatory Material Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup-si, Jeonbuk 56212, Korea.
Korea Research Institute of Bioscience and Biotechnology · KRChonnam National University · KRDaegu Haany University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have reported the biological activities of retrofractamide C (RAC). However, few studies have investigated the anti-inflammatory effect of RAC. In the present study, we investigated the anti-inflammatory effect of RAC using lipopolysaccharide (LPS)-induced J774A.1 cells and a xylene-induced mouse ear edema model. Treatment with RAC decreased LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) secretion and inducible NO synthase (iNOS) and cyclooxygenase 2 (COX2) protein expression. It also downregulated the LPS-induced production of interleukin-1β (IL-1β) and interleukin-6 (IL-6) but not tumor necrosis factor α (TNF-α). In the LPS-induced signaling pathway, RAC inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) but not c-Jun N-terminal kinase (JNK) or p38. In a xylene-induced mouse ear edema model, RAC treatment alleviated edema formation and inflammatory cell infiltration. In conclusion, the present study indicates that RAC has the potential to have anti-inflammatory effects and could be a prospective functional food.

Indexed as

AmidesAnimalsCell LineCyclooxygenase 2DinoprostoneEarEdemaExtracellular Signal-Regulated MAP KinasesGene Expression RegulationInflammation MediatorsInterleukin-1betaInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesMaleMice, Inbred ICRAmidesCyclooxygenase 2DinoprostoneExtracellular Signal-Regulated MAP KinasesInflammation MediatorsInterleukin-1betaInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alphaXylenesanti-inflammationPiper longumretrofractamide Cxylene-induced ear edema

Identifiers

PMID32899525
PMCPMC7570867
OpenAlexW3083014380

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.