| Summary: | 碩士 === 臺北醫學大學 === 保健營養學系 === 91 === The purpose of this study was to investigate the effects of EGb761 containing 22-27% ginkgo-flavone glycosides and 5-7% terpenoids on hepatocelluarlar carcinoma. In the in vitro experiment, EGb761 was added by different concentrations (0-1000 μg/mL) in the medium of human hepatocelluarlar carcinoma (HCC) cell lines (HepG2 and Hep3B2.1-7) for 24 to 48 hours. The effects of EGb761 on cell proliferation and lactate dehydrogenase (LDH) leakage in HepG2 and Hep3B2.1-7 cells and the expression of p53 and proliferating cell nuclear antigen (PCNA) in HepG2 cells were determined. The results showed that EGb761 (50-1000 μg/mL) significantly suppressed cell proliferation and increased LDH leakage of HepG2 and Hep3B2.1-7 cells (p < 0.05). Cell proliferation of HepG2 and Hep3B2.1-7cells treated with EGb761 (1000 μg/mL) was 45.3% and 38.8% of the control (p < 0.05), respectively. LDH leakage of HepG2 cells without EGb761 and with EGb761 (1000 μg/mL) was 6.7% and 37.7%, respectively, and that of Hep3B2.1-7cells without EGb761 and with EGb761 (1000 μg/mL) was 7.2% and 40.3%, respectively. The expression of p53 and PCNA proteins in HepG2 cells treated with EGb761 (1000 μg/mL) was 173.7% and 85.1%, respectively. In the in vivo experiment, Fischer 344 (F344) rats were randomly divided into four groups: control (no HCC without EGb761), no HCC with EGb761, HCC without EGb761, and HCC with EGb761 groups. HCC rats were induced by the 3-stage model of diethylnitrosamine (DEN)－2-acetylaminofluorene (2-AAF)－partial hepatectomy (a left-leaf liver resection) for five weeks. After HCC induction, rats were fed with EGb761 (50 mg/kg body weight/day) for four weeks to grossly evaluate cell proliferation by pathological assessment. The results showed that liver weight and food intake during the experimental period did not differ among the groups. Body weight gain of the control group was significantly higher than that of the HCC groups (p < 0.05). The maximal area and number of nodules did not significantly differ between the HCC groups with and without EGb761. In conclusion, EGb761 significantly suppressed proliferation and reduced viability of HepG2 and Hep3B2.1-7 cells, increased p53 expression and decreased PCNA expression in HepG2 cell in vitro. The in vivo experiment showed that rats with HCC had significantly lower weight gain. The pathological assessment showed that EGb761 treatment (50 mg/kg body weight/day) for 4 weeks did not obviously improve HCC.
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