Mobile website
Basic Research
Salvianolate induces apoptosis of human hepatoma SMMC-7721 cells through mitochondrial pathway
- Article
- Figures
- Metrics
- Preview PDF
- Reference
- Related
- Cited by
- Materials
Abstract:
Objective:To explore the apoptosisinducing effect of salvianolate on hepatoma SMMC7721 cells and the underlying mechanism. Methods:SMMC7721 cells were cocultured in vitro with different concentrations (0.5, 1, 2 mg/ml) of salvianolate for 24 h. The apoptotic SMMC7721 cells were examined by flow cytometry, and the changes of mitochondrial transmembrane potential were examined by mitochondrial transmembrane potential JC1 kit. The activities of caspase8, caspase9, and caspase3 were detected by spectrophotometry in the hepatoma SMMC7721 cells after cocultured with 1 mg/ml salvianolate. The changes of apoptotic SMMC7721 cells induced by salvianolate in the presence or absence of caspase9 inhibitor or caspase3 inhibitor were measured by flow cytometry. The expressions of proapoptotic protein Bax and antiapoptotic protein Bcl2 were detected by Western blotting analysis. Results:Salvianolate significantly induced apoptosis of hepatoma SMMC7721 cells (P<0.05), and the decline of mitochondrial membrane potential increased with the increase of salvianolate concentration (P<0.05). The activities of caspase9 and caspase3, but not caspase8, were increased in hepatoma cells after treatment with 1 mg/ml salvianolate for 24 h (P<0.05). The apoptosisinducing effect of salvianolate was significantly decreased in the presence of caspase9 or caspase3 inhibitors (P<005). Western blotting results showed that salvianolate increased proapoptotic protein Bax expression and decreased antiapoptotic protein Bcl2 expression. Conclusion:Salvianolate can induce the apoptosis of human hepatoma SMMC7721 cells in a dosedependent manner, which is probably mediated by mitochondrial apoptosis pathway.
Keywords:
Project Supported:
Project supported by the Youth Research Program of Shanghai Health Bureau (No. 2008Y085), and the National Science and Technology Supporting Program of the Ministry of Health (No. 2008BAI60B03)
Clc Number:
