Evidence map›Paper›PMID 25400762›Full record

ArticleInternational journal of clinical and experimental pathology2014

Mechanism of the promotion of steatotic HepG2 cell apoptosis by cholesterol.

Chunyan Zhu, Ping Xie, Fei Zhao, Lingqiang Zhang, Wei An, Yutao Zhan

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Apoptosis and non-alcoholic fatty liver diseases.World journal of gastroenterology · 2018
    Review
  9. Ethanol extract ofNutrition research and practice · 2018
    Article
  10. Article
  11. Review
  12. Glycosyltransferases and non-alcoholic fatty liver disease.World journal of gastroenterology · 2016
    Review
  13. Article
  14. 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 3 institutions in 2 countries.

Chunyan ZhuDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University Beijing 100730, China.
Ping XieState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine Beijing 102206, China.
Fei ZhaoDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University Beijing 100730, China.
Lingqiang ZhangState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine Beijing 102206, China.
Wei AnDepartment of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University Beijing 100069, China.
Yutao ZhanDepartment of Gastroenterology, Beijing Tongren Hospital, Capital Medical University Beijing 100730, China.
Beijing Tongren Hospital · CNBeijing Proteome Research Center · CNCells Therapy (Poland) · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of cholesterol in the pathogenesis of non-alcoholic steatohepatitis (NASH) remains unclear. It is known that apoptosis of hepatocytes is an important characteristics of NASH. The objective of this study was to investigate the effects of cholesterol on steatotic HepG2 cell apoptosis and the possible mechanism in vitro. In this study, HepG2 cells were divided into three groups: (1) normal group, (2) steatosis group and (3) cholesterol group. HepG2 cells were treated with oleic acid to establish a steatosis study model. Steatosis was assessed by Oil Red O staining and triglyceride content assay. Cell apoptosis was measured using an apoptosis kit. The expression levels of apoptosis-related proteins (P53, Bcl-2, Bax, caspase-3, cyclin A, cyclin B1 and cyclin E) were determined by western blot analyses. We found that a hepatocyte steatosis model was successfully established by oleic acid (200 μmol/L) induction. The cholesterol (50 mg/L) group had similar amount of lipid droplets and triglyceride content as steatosis group (P > 0.5). However, the apoptosis rate (P < 0.01) of the cholesterol group was significantly higher than that of the normal group or the steatosis group, and the protein expressions of Bax and caspase-3, but not P53, Bcl-2, cyclin A, cyclin B1 and cyclin E, were also increased in the cholesterol group. Those results suggested that cholesterol markedly promoted apoptosis of steatosis HepG2 cells in vitro, likely through the up-regulation of Bax and caspase-3 expression. This study contributes to explain the effect of cholesterol on NASH pathogenesis.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCell Cycle ProteinsCholesterolHep G2 CellsHumansLipid MetabolismLiverNon-alcoholic Fatty Liver DiseaseOleic AcidSignal TransductionApoptosis Regulatory ProteinsCell Cycle ProteinsCholesterolOleic AcidapoptosisCholesterolHepG 2 cellssteatosis

Identifiers

PMID25400762
PMCPMC4230101
OpenAlexW1783951946

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.