Evidence map›Paper›PMID 27106477›Full record

ArticleInflammation2016

Paeonol Inhibits Lipopolysaccharide-Induced HMGB1 Translocation from the Nucleus to the Cytoplasm in RAW264.7 Cells.

Hang Lei, Quan Wen, Hui Li, Shaohui Du, Jing-Jing Wu, Jing Chen, Haiyuan Huang, Dongfeng Chen, Yiwei Li, Saixia Zhang and 3 more

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Paeonol inhibits proliferation and induces cell apoptosis of human T24 and 5637 bladder cancer cells in vitro and in vivo.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  5. Paeonol attenuates inflammation by confining HMGB1 to the nucleus.Journal of cellular and molecular medicine · 2021
    Article
  6. Evidence-based complementary and alternative medicine : eCAM · 2020
    Review
  7. Article
  8. Article
  9. Review
  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

13 authors at 3 institutions in 2 countries.

Hang LeiLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Quan WenLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Hui LiLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China. lihui@gzucm.edu.cn.
Shaohui DuDepartment of Internal Medicine, Affiliated Shenzhen Hospital to Guangzhou University of Chinese Medicine, No. 2 Fuhua Road, 51803, Shenzhen, China.
Jing-Jing WuLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Jing ChenLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Haiyuan HuangLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Dongfeng ChenLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Yiwei LiLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Saixia ZhangLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Jianhong ZhouLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Rudong DengLaboratory of Molecular Medicine, School of Basic Medicine, Guangzhou University of Chinese Medicine, 232 Waihuandong Road, Guangzhou University Town, Guangzhou, 510006, China.
Qinglin YangDepartment of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Blvd, Webb 435, Birmingham, AL, 35242, USA.
Guangzhou University of Chinese Medicine · CNTwelfth Guangzhou City People's Hospital · CNUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transport of high-mobility group box 1 (HMGB1), a highly conserved non-histone DNA-binding protein, from the nucleus to the cytoplasm is induced by lipopolysaccharide (LPS). Secretion of HMGB1 appears to be a key lethal factor in sepsis, so it is considered to be a therapeutic target. Previous studies have suggested that paeonol (2'-hydroxy-4'-methoxyacetophenone), an active compound of Paeonia lactiflora Pallas, exerts anti-inflammatory effects. However, the effect of paeonol on HMGB1 is unknown. Here, we investigated the effect of paeonol on the expression, location, and secretion of HMGB1 in LPS-induced murine RAW264.7 cells. ELISA revealed HMGB1 supernatant concentrations of 615 ± 30 ng/mL in the LPS group and 600 ± 45, 560 ± 42, and 452 ± 38 ng/mL in cells treated with 0.2, 0.6, or 1 mM paeonol, respectively, suggesting that paeonol inhibits HMGB1 secretion induced by LPS. Immunohistochemistry and Western blotting revealed that paeonol decreased cytoplasmic HMGB1 and increased nuclear HMGB1. Chromatin immunoprecipitation microarrays suggested that HMGB1 relocation to the nucleus induced by paeonol might depress the action of Janus kinase/signal transducers and activators of transcription, chemokine, and mitogen-activated protein kinase pro-inflammatory signaling pathways. Paeonol was also found to inhibit tumor necrosis factor-α promoter activity in a dose-dependent manner. These results indicate that paeonol has the potential to be developed as a novel HMGB1-targeting therapeutic drug for the treatment of inflammatory diseases.

Indexed as

AcetophenonesAnimalsAnti-Inflammatory AgentsCell NucleusCytoplasmHMGB1 ProteinLipopolysaccharidesMicePromoter Regions, GeneticProtein TransportRAW 264.7 CellsTumor Necrosis Factor-alphaAcetophenonesAnti-Inflammatory AgentsHMGB1 ProteinLipopolysaccharidespaeonolTumor Necrosis Factor-alphahigh-mobility group box 1inflammatory factorlipopolysaccharidepaeonolsepsis

Identifiers

PMID27106477
OpenAlexW2336271794

What OpenQuestion holds

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Read underepoch 390

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.