论文部分内容阅读
Objective:To confirm the anticancer effect of total annonaceous acetogenins(TAAs)abstracted from Annona squamosa Linn,on human hepatocarcinoma.Methods:The inhibitory effect of TAAs was demonstrated in H_(22)-bearing mice.The potency of TAAs was confirmed as its 50%inhibiting concentration(IC_(50))on Bel-7402 cell under Sulfur Rhodamine B staining.Both underlying mechanisms were explored as cellular apoptosis and cell cycle under flow cytometry.Mitochondrial and recipient apoptotic pathways were differentiated as mitochondrial membrane potential under flow cytometry and caspases activities under fluorescence analysis.Results:The inhibitory rate of TAAs in mice was 50.98%at 4 mg/kg dose.The IC_(50)of TAAs on Bel-7402 was20.06μg/mL(15.13-26.61μg/mL).Effective mechanisms of TAAs were confirmed as both of arresting cell cycle at G_1 phase and inducing apoptosis dose-and time-dependently.Mitochondrial and recipient pathways involved in apoptotic actions of TAAs.Conclusion:TAAs is effective for hepatocarcinoma,via inhibiting proliferation and inducing apoptosis.
Objective: To confirm the anticancer effect of total annonaceous acetogenins (TAAs) abstracted from Annona squamosa Linn, on human hepatocarcinoma. Methods: The inhibitory effect of TAAs was demonstrated in H_ (22) -bearing mice. Potency of TAAs was confirmed as its 50% inhibiting concentration (IC 50) on Bel-7402 cell under Sulfur Rhodamine B staining. Both underlying mechanisms were explored as cellular apoptosis and cell cycle under flow cytometry. Mitochondrial and recipient apoptotic pathways were differentiated as mitochondrial membrane potential under flow cytometry Results: The inhibitory rate of TAAs in mice was 50.98% at 4 mg / kg dose.The IC 50 of TAAs on Bel-7402 was 20.06 μg / mL (15.13-26.61 μg / mL) . Effective mechanisms of TAAs were arrested as both as arresting cell cycle at G_1 phase and inducing apoptosis dose-and time-dependently. Mitochondrial and recipient pathways involved in apoptotic actions of TAAs. Conlusion: TAAs is effective for hepatocarcinoma, via inhibiting proliferation and inducing apoptosis.