Magnolol 對人類肝癌細胞之抗肝癌活性的機制研究 Studies on the Mechanisms of Magnolol-Induced Anti-tumoral activity in Human Hepatoma Cells.
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The objective of this thesis research is to investigate the anti-tumoral action of magnolol on the hepatoma cell line Hep-G2 and its underlying molecular mechanisms. In vitro studies demonstrated that magnolol at low concentrations (10~50 μM) induced a dose-dependent inhibition of Hep-G2 growth and cell cycle arrest. On the other hand, magnolol at a higher concentration (100 μM) induced an apoptosis of Hep-G2 cells. However, magnolol at these concentrations had no effect on human untransformed cells, such as human fibroblasts and human umbilical venous endothelial cells (HUVEC). Western blot analysis demonstrates that an increased expression of cyclin-dependent kinase (CDK) inhibitor, p21, is the major factor contributing the magnolol-mediated cell cycle arrest. Treatment of Hep-G2 with 100 μM magnolol caused DNA fragmentation and sub-G0/G1 peak at 72 hours when the cell was grown in the culture medium containing 10 % fetal bovine serum. Several apoptosis-related proteins including caspase 8 were shown to be activated in response to magnolol treatment in Hep-G2. Administration of Fas antagonist antibody (ZB4), which neutralized the Fas receptor, prevented the magnolol-mediated caspase 8 cleavage and suppressed the magnolol-induced apoptosis. This result suggests that Fas receptor may be involved, at least partially, in the magnolol-induced apoptosis.In conclusion, our data demonstrated that magnolol at low concentrations (10-50 μM) induced an anti-proliferation of Hep-G2 and at a higher concentration (100 μM) caused apoptosis. Only when the mechanism of its effect is fully understood can we begin to design a strategy to use magnolol for anti-cancer therapy.