Run-mei Yang1, Wen-min Li1, Wei-jun Hu2, Wen-hua Huang1, Chun-yan Zhu1, Jing-guang Yu1, Xin Zhao1, Da-yong Cai1, Nan-nan Gao3. 1. Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100193, China. 2. Henan Institute of Engineering, Zhengzhou, 451191, China. 3. Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100193, China. gaonann@126.com.
Abstract
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 H22-bearing mice. The potency of TAAs was confirmed as its 50% inhibiting concentration (IC50) 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 IC50 of TAAs on Bel-7402 was 20.06 µg/mL (15.13-26.61µg/mL). Effective mechanisms of TAAs were confirmed as both of arresting cell cycle at G1 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 H22-bearing mice. The potency of TAAs was confirmed as its 50% inhibiting concentration (IC50) 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 IC50 of TAAs on Bel-7402 was 20.06 µg/mL (15.13-26.61µg/mL). Effective mechanisms of TAAs were confirmed as both of arresting cell cycle at G1 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.
Authors: José R Tormo; Nuria DePedro; Inmaculada Royo; Isabel Barrachina; M Carmen Zafra-Polo; Cristina Cuadrillero; Pilar Hernández; Diego Cortes; Fernando Peláez Journal: Oncol Res Date: 2005 Impact factor: 5.574