Magnolol抑制人類肝癌細胞Hep-3B增生的分子機轉 Molecular Mechanisms of Magnolol-Induced Antiproliferation effect in Hep-3B cells.
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The aim of this study is to investigate the antiproliferation effect of magnolol on the human hepatoma cell line Hep-3B (p53 null) and its underlying molecular mechanisms. Magnolol is one of the phenolic pure compounds isolated from the bark of Hou pu’ (Cortex Magnolia officina1is), which has been commonly used in Chinese herb medicine in the treatment of fever, headache, anxiety, diarrhea and stroke.In vitro studies, we showed that magnolol at low concentrations (10~50 M) induced a dose-dependent inhibition of cell growth in Hep-3B. However, magnolol at a higher concentration (100 M) induced the occurrence of apoptosis. To study further the molecular mechanisms of anti-liver cancer effect of magnolol, we analyzed the cell population during cell cycle by [3H]thymidine incorporation and flow cytometry analyses, and detected the expression levels of cell cycle regulatory proteins by using western blot analysis. Treatment of Hep-3B cells with magnolol (10-50 M) induced a decrease in DNA systhesis and retardation of cell cycle at G0/G1 phase of cell cycle. The protein levels of cyclins and CDKs were not changed significantly in the magnolol-treated Hep-3B cells as compared with the control cells. However, the p21 protein was upregulated during magnolol-mediated antiproliferation, and downregulated during magnolol-induced apoptosis. Moreover, the CDK2, but not CDK4, kinase activity was downregulated in the magnolol-treated Hep-3B in a dose-dependent manner. For the molecular mechanisms involved in the magnolol-induced apoptosis in Hep-3B, we observed that intracellular events included (1) degradation of bax and (2) activation of caspases 3, 8, and 9.