Evidence map›Paper›PMID 19317806›Full record

ArticleCell proliferation2009

Silymarin inhibited proliferation and induced apoptosis in hepatic cancer cells.

G Ramakrishnan, L Lo Muzio, C M Elinos-Báez, S Jagan, T A Augustine, S Kamaraj, P Anandakumar, T Devaki

Abstract read
In one paragraph

Article in Cell proliferation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Formulation of silymarin surface modified vesicles: In vitro characterization to cell viability assessment.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. A review of therapeutic potentials of milk thistle (Iranian journal of basic medical sciences · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Changes in Glutathione Content in Liver Diseases: An Update.Antioxidants (Basel, Switzerland) · 2021
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 2 countries.

G RamakrishnanDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, Tamil Nadu, India.
L Lo Muzio
C M Elinos-Báez
S Jagan
T A Augustine
S Kamaraj
P Anandakumar
T Devaki
University of Madras · INUniversity of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe aim of this study was to investigate mechanisms involved in the growth inhibitory effect of silymarin, in humanhepatocellular carcinoma. MATERIALS AND

methodsThe human hepatocellular carcinoma cell line HepG2 was utilized and the MTT assay was performed to study the antiproliferative effect of silymarin. Dual staining was undertaken for ethidium bromide/acridine orange, propidium iodide staining and DNA fragmentation studies were executed to confirm the presence of apoptosis. Cell-cycle analysis was revealed by flow cytometry and mitochondrial transmembrane potential was measured by uptake of the mitochondrial-specific lipophilic cationic dye rhodamine 123. Western blotting analysis for cytochrome c, p53, Bax, Bcl-2, APAF-1, caspase-3, survivin, beta-catenin, cyclin D1, c-Myc and PCNA was carried out.

resultsSilymarin inhibited population growth of the hepatocellular carcinoma cells in a dose-dependent manner, and the percentage of apoptotic cells was increased after treatment with 50 and 75 microg/ml silymarin for 24 h. Silymarin treatment increased the proportion of cells with reduced DNA content (sub-G(0)/G(1) or A(0) peak), indicative of apoptosis with loss of cells in the G(1) phase. Silymarin also decreased mitochondrial transmembrane potential of the cells, thereby increasing levels of cytosolic cytochrome c while up-regulating expression of pro-apoptotic proteins (such as p53, Bax, APAF-1 and caspase-3) with concomitant decrease in anti-apoptotic proteins (Bcl-2 and survivin) and proliferation-associated proteins (beta-catenin, cyclin D1, c-Myc and PCNA).

conclusionsOur results demonstrate that silymarin treatment inhibited proliferation and induced apoptosis in the human hepatocellular carcinoma cell line HepG2.

Indexed as

ApoptosisApoptotic Protease-Activating Factor 1bcl-2-Associated X Proteinbeta CateninCaspase 3Cell CycleCell Line, TumorCell NucleusCell ProliferationCyclin D1Cytochromes cDNA FragmentationDose-Response Relationship, DrugFlavonoidsGene ExpressionHumansAPAF1 protein, humanApoptotic Protease-Activating Factor 1bcl-2-Associated X Proteinbeta CateninBIRC5 protein, humanCaspase 3CCND1 protein, humanCyclin D1Cytochromes cFlavonoidsInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycSilymarinSurvivinTumor Suppressor Protein p53

Identifiers

PMID19317806
PMCPMC6495958
OpenAlexW2170028652

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.