Evidence map›Paper›PMID 32596881›Full record

ArticleJournal of cellular and molecular medicine2020

Salvianic acid A alleviates chronic alcoholic liver disease by inhibiting HMGB1 translocation via down-regulating BRD4.

Yanwen Lan, Ran Yan, Wen Shan, Junyi Chu, Ruimin Sun, Ruiwen Wang, Yan Zhao, Zhanyu Wang, Ning Zhang, Jihong Yao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. 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
1.0field-weighted citation impact, top 28% 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, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022
    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

10 authors at 1 institution in 1 country.

Yanwen LanDepartment of Pharmacy, The Second Hospital of Dalian Medical University, Dalian, China.
Ran YanDepartment of Pharmacy, The Second Hospital of Dalian Medical University, Dalian, China.
Wen ShanDepartment of Pharmacy, The Second Hospital of Dalian Medical University, Dalian, China.
Junyi ChuDepartment of Pharmacy, The Second Hospital of Dalian Medical University, Dalian, China.
Ruimin SunDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Ruiwen WangDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Yan ZhaoDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Zhanyu WangDepartment of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Ning ZhangDepartment of Pharmacy, The Second Hospital of Dalian Medical University, Dalian, China.ORCID 0000-0002-8376-1037
Jihong YaoDepartment of Pharmacology, Dalian Medical University, Dalian, China.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is the major cause of chronic liver disease and a global health concern. ALD pathogenesis is initiated with liver steatosis, and ALD can progress to steatohepatitis, fibrosis, cirrhosis and even hepatocellular carcinoma. Salvianic acid A (SAA) is a phenolic acid component of Danshen, a Chinese herbal medicine with possible hepatoprotective properties. The purpose of this study was to investigate the effect of SAA on chronic alcoholic liver injury and its molecular mechanism. We found that SAA significantly inhibited alcohol-induced liver injury and ameliorated ethanol-induced hepatic inflammation. These protective effects of SAA were likely carried out through its suppression of the BRD4/HMGB1 signalling pathway, because SAA treatment largely diminished alcohol-induced BRD4 expression and HMGB1 nuclear translocation and release. Importantly, BRD4 knockdown prevented ethanol-induced HMGB1 release and inflammatory cytokine production in AML-12 cells. Similarly, alcohol-induced pro-inflammatory cytokines were blocked by HMGB1 siRNA. Collectively, our results reveal that activation of the BRD4/HMGB1 pathway is involved in ALD pathogenesis. Therefore, manipulation of the BRD4/HMGB1 pathway through strategies such as SAA treatment holds great therapeutic potential for chronic alcoholic liver disease therapy.

Indexed as

AnimalsBromodomain Containing ProteinsCell NucleusCells, CulturedCytokinesDown-RegulationHMGB1 ProteinInflammationLactatesLiverLiver Diseases, AlcoholicMaleMiceNuclear ProteinsProtective AgentsRats3,4-dihydroxyphenyllactic acidBrd4 protein, ratBromodomain Containing ProteinsCytokinesHbp1 protein, ratHMGB1 ProteinLactatesNuclear ProteinsProtective AgentsTranscription Factorsalcoholic liver diseaseBRD4HMGB1inflammationSAA

Identifiers

PMID32596881
PMCPMC7412690
OpenAlexW3037999382

What OpenQuestion holds

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LicenceCC BY
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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.