Evidence map›Paper›PMID 25882312›Full record

ArticleJournal of ethnopharmacology2015

Identifying panaxynol, a natural activator of nuclear factor erythroid-2 related factor 2 (Nrf2) from American ginseng as a suppressor of inflamed macrophage-induced cardiomyocyte hypertrophy.

Chen Qu, Bin Li, Yimu Lai, Hechu Li, Anthony Windust, Lorne J Hofseth, Mitzi Nagarkatti, Prakash Nagarkatti, Xing Li Wang, Dongqi Tang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ethnopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
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  11. Terpenoids, Cannabimimetic Ligands, beyond theMolecules (Basel, Switzerland) · 2020
    Review
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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

13 authors.

Chen QuDepartment of Breast and Thyroid Surgery, Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China; Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Bin LiShandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital of Shandong University, Jinan 250012, China; Department of Reproductive Medicine, Linyi People׳s Hospital, Linyi, Shandong 276003, China.
Yimu LaiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Hechu LiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Anthony WindustMeasurement Science and Standards, National Research Council, Ottawa, Canada.
Lorne J HofsethDepartment of Pharmaceutical and Biomedical Sciences, South Carolina College of Pharmacy, Columbia, SC 29208, USA.
Mitzi NagarkattiDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Prakash NagarkattiDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Xing Li WangShandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital of Shandong University, Jinan 250012, China.
Dongqi TangShandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital of Shandong University, Jinan 250012, China.
Joseph S JanickiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29208, USA.
Xingsong TianDepartment of Breast and Thyroid Surgery, Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China. Electronic address: txs0509@163.com.
Taixing CuiDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29208, USA; Shandong University Qilu Hospital Research Center for Cell Therapy, Key Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital of Shandong University, Jinan 250012, China. Electronic address: taixing.cui@uscmed.sc.edu.

Funding

Targeting early ceramide elevation in pre-symptomatic eczemaP20GM103641 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ENOS, REILLY, NAGARKATTI, PRAKASH S · 2012 to 2023
$20.7M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
Role of natural indoles in experimental autoimmune encephalomyelitisR01AT006888 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI · 2011 to 2015
$2.0M
NCCIH NIH HHS 2P01AT003961-06A1NCCIH NIH HHS P01 AT003961NCCIH NIH HHS R01 AT006888NIGMS NIH HHS P020GM103641NIGMS NIH HHS P20 GM103641
6 · The paper itself

Abstract

ethnopharmacological relevanceAmerican ginseng is capable of ameliorating cardiac dysfunction and activating Nrf2, a master regulator of antioxidant defense, in the heart. This study was designed to isolate compounds from American ginseng and to determine those responsible for the Nrf2-mediated resolution of inflamed macrophage-induced cardiomyocyte hypertrophy. MATERIALS AND

methodsA standardized crude extract of American ginseng was supplied by the National Research Council of Canada, Institute for National Measurement Standards. A bioassay-based fractionization of American ginseng was performed to identify the putative substances which could activate Nrf2-mediated suppression of pro-inflammatory cytokine expression in macrophages and macrophage-mediated pro-hypertrophic growth in cardiomyocytes.

resultsA hexane fraction of an anti-inflammatory crude extract of American ginseng was found to be most effective in suppressing the inflammatory responses in macrophages. Preparative, reverse-phase HPLC and a comparative analysis by analytical scale LC-UV/MS revealed the hexane fraction contains predominantly C17 polyacetylenes and linolenic acid. Panaxynol, one of the major polyacetylenes, was found to be a potent Nrf2 activator. Panaxynol posttranscriptionally activated Nrf2 by inhibiting Kelch-like ECH-associated protein (Keap) 1-mediated degradation without affecting the binding of Keap1 and Nrf2. Moreover, panaxynol suppressed a selected set of cytokine expression via the activation of Nrf2 while minimally regulating nuclear factor-kappa B (NF-κB)-mediated cytokine expression in macrophages. It also dramatically inhibited the inflamed macrophage-mediated cardiomyocyte death and hypertrophy by activating Nrf2 in macrophages.

conclusionsThese results demonstrate that American ginseng-derived panaxynol is a specific Nrf2 activator and panaxynol-activated Nrf2 signaling is at least partly responsible for American ginseng-induced health benefit in the heart.

Indexed as

PanaxAnimalsAnti-Inflammatory AgentsCell LineCytokinesDiynesFatty AlcoholsFemaleHypertrophyMacrophagesMaleMice, KnockoutMyocytes, CardiacNF-E2-Related Factor 2Nitric Oxide Synthase Type IIPlant ExtractsAnti-Inflammatory AgentsCytokinesDiynesfalcarinolFatty AlcoholsNF-E2-Related Factor 2Nitric Oxide Synthase Type IINos2 protein, mousePlant ExtractsAmerican ginsengCardiomyocytesInflammationMacrophagesNrf2Panaxynol

Identifiers

PMID25882312
PMCPMC4810680

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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.