OBJECTIVES: To investigate the radiosensitizing effects of Radix Angelicae Sinensis-Radix Hedysari (RAS-RH [an ultra-filtration extract]) and its underlying mechanisms in human liver cancer cells H22. METHODS: This study was conducted between September 2010 and August 2012 in the Gansu University of Traditional Chinese Medicine, Lanzhou, China. The groups were assigned as the control group, drug (RAS-RH) group, 12C6+ radiation group, and combination group. The cell counting kit-8 assay, colony formation assay, cell cycle changes, and apoptosis analysis were carried out, and survivin and casepase-9 were evaluated by reverse transcription polymerase chain reaction and Western blot analyses in the 4 groups. RESULTS: The inhibitory effect of RAS-RH on H22 cells was dependent on both concentration and time, RAS-RH was able to enhance the radiosensitivity of H22 cells by increasing cell survival fraction and radiosensitization parameters. Apoptosis and the gap2/mitosis (G2/M) phase transition induced by 12C6+ heavy ion radiation was enhanced by RAS-RH treatment. Irradiation, combined with RAS-RH, decreased survivin expression while increasing casepase-9 expression in H22 cells. CONCLUSION: The RAS-RH increased the radiosensitivity of H22 cells of 12C6+ heavy ion radiation significantly, and its possible mechanism of radiosensitization is to enhance caspase-dependent apoptosis through the down-regulation of survivin, thus, it can be used as an effective radiosensitizer.
OBJECTIVES: To investigate the radiosensitizing effects of Radix Angelicae Sinensis-Radix Hedysari (RAS-RH [an ultra-filtration extract]) and its underlying mechanisms in humanliver cancer cells H22. METHODS: This study was conducted between September 2010 and August 2012 in the Gansu University of Traditional Chinese Medicine, Lanzhou, China. The groups were assigned as the control group, drug (RAS-RH) group, 12C6+ radiation group, and combination group. The cell counting kit-8 assay, colony formation assay, cell cycle changes, and apoptosis analysis were carried out, and survivin and casepase-9 were evaluated by reverse transcription polymerase chain reaction and Western blot analyses in the 4 groups. RESULTS: The inhibitory effect of RAS-RH on H22 cells was dependent on both concentration and time, RAS-RH was able to enhance the radiosensitivity of H22 cells by increasing cell survival fraction and radiosensitization parameters. Apoptosis and the gap2/mitosis (G2/M) phase transition induced by 12C6+ heavy ion radiation was enhanced by RAS-RH treatment. Irradiation, combined with RAS-RH, decreased survivin expression while increasing casepase-9 expression in H22 cells. CONCLUSION: The RAS-RH increased the radiosensitivity of H22 cells of 12C6+ heavy ion radiation significantly, and its possible mechanism of radiosensitization is to enhance caspase-dependent apoptosis through the down-regulation of survivin, thus, it can be used as an effective radiosensitizer.