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Silymarin inhibited proliferation and induced apoptosis in hepatic cancer cells
G Ramakrishnan1, L Lo Muzio, C M Elinos-Báez
1Department of Biochemistry, University of Madras, Guindy Campus, Chennai, Tamil Nadu, India.
Objectives:
The aim of this study was to investigate mechanisms involved in the growth inhibitory effect of silymarin, in humanhepatocellular carcinoma.
Materials And Methods:
The 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.
Results:
Silymarin 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).
Conclusions:
Our results demonstrate that silymarin treatment inhibited proliferation and induced apoptosis in the human hepatocellular carcinoma cell line HepG2.
Insights
Silymarin inhibits growth and triggers apoptosis in human hepatocellular carcinoma cells. This natural compound affects cell cycle, mitochondrial potential, and key proteins involved in cell death and proliferation.
Area of Science:
- Hepatocellular carcinoma research
- Pharmacology
- Molecular biology
Background:
- Hepatocellular carcinoma (HCC) is a major global health concern.
- Silymarin, a natural compound, has shown potential anticancer properties.
Purpose of the Study:
- To investigate the mechanisms behind silymarin's growth inhibitory effects on human HCC.
- To elucidate the role of apoptosis induction by silymarin in HCC.
Main Methods:
- Utilized the HepG2 human HCC cell line.
- Assessed antiproliferative effects using MTT assay.
- Confirmed apoptosis via dual staining, DNA fragmentation, cell cycle analysis, and Western blotting for key proteins.
Main Results:
- Silymarin demonstrated dose-dependent inhibition of HCC cell growth.
- Induced apoptosis, evidenced by increased apoptotic cells, sub-G(0)/G(1 DNA content, and decreased mitochondrial potential.
- Modulated protein expression, upregulating pro-apoptotic factors (p53, Bax, APAF-1, caspase-3) and downregulating anti-apoptotic (Bcl-2, survivin) and proliferation proteins (beta-catenin, cyclin D1, c-Myc, PCNA).
Conclusions:
- Silymarin effectively inhibits proliferation in HepG2 cells.
- Silymarin treatment induces apoptosis through intrinsic and extrinsic pathways in HCC.
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