Evidence map›Paper›PMID 26412258›Full record

ArticleInflammation2016

Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways.

Chang-Bum Ahn, Won-Kyo Jung, Sun-Joo Park, Yong-Tae Kim, Won-Suk Kim, Jae-Young Je

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 95 citations in OpenAlex.

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  10. Review
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  12. Pharmaceutics · 2022
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  16. The potential of BEN815 as an anti-inflammatory, antiviral and antioxidant agent for the treatment of COVID-19.Phytomedicine plus : international journal of phytotherapy and phytopharmacology · 2021
    Article
  17. Lotus seeds (Food science & nutrition · 2021
    Review
  18. Article
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  20. Dietary Supplementation with Sea Bass (International journal of molecular sciences · 2019
    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 at 4 institutions in 1 country.

Chang-Bum AhnDivision of Food and Nutrition, Chonnam National University, Gwangju, 550-757, Republic of Korea.
Won-Kyo JungDepartment of Biomedical Engineering, Pukyong National University, Busan, 608-737, Republic of Korea.
Sun-Joo ParkDepartment of Chemistry, Pukyong National University, Busan, 608-737, Republic of Korea.
Yong-Tae KimDepartment of Food Science and Biotechnology, Kunsan National University, Kunsan, 573-701, Republic of Korea.
Won-Suk KimMajor in Pharmaceutical Engineering, Division of Bioindustry, Silla University, Busan, 46958, Republic of Korea.
Jae-Young JeDepartment of Marine-Bio Convergence Science, Pukyong National University, Busan, 608-739, Republic of Korea. jjy1915@pknu.ac.kr.ORCID http://orcid.org/0000-0002-4800-0566
Pukyong National University · KRChonnam National University · KRKunsan National University · KRSilla University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chitosan is a naturally occurring polysaccharide, which has exhibited antioxidant, antimicrobial, and anti-cancer activities among others. Modification of chitosan by grafting phenolic compounds is a good strategy for improvement of bioactivities of chitosan. We investigated the anti-inflammatory action of gallic acid-grafted-chitosan (GAC) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. GAC inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 macrophages. GAC also suppressed the production and mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). GAC inactivated nuclear factor-κB (NF-κB) via inhibiting the phosphorylation and degradation of the NF-κB inhibitor, IκB. In addition, GAC suppresses the activation of activator protein-1 (AP-1) through the phosphorylation of mitogen-activated protein kinase (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results suggest that GAC has the potential anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through MAPK signaling pathways.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineChitosanCyclooxygenase 2DinoprostoneEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGallic AcidI-kappa B KinaseInflammationInterleukin-1betaInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesMacrophagesAnti-Inflammatory AgentsChitosanCyclooxygenase 2DinoprostoneExtracellular Signal-Regulated MAP KinasesGallic Acidgallic acid-g-chitosanI-kappa B KinaseIL1B protein, mouseInterleukin-1betaInterleukin-6JNK Mitogen-Activated Protein KinasesLipopolysaccharidesNitric OxideNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesPtgs2 protein, mouseRela protein, mouseTranscription Factor AP-1Transcription Factor RelATumor Necrosis Factor-alphaAP-1chitosaninflammationMAPKNF-κBRAW macrophage

Identifiers

PMID26412258
OpenAlexW2188591325

What OpenQuestion holds

Textmetadata
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.