Previously we demonstrated that CCY1a-E2 was the most potent derivative of benzyloxybenzaldehyde and it inhibited growth of leukemia cells by induction of cell cycle arrest and apoptosis. In this study, our data showed that CCY1a-E2 also inhibited the proliferation of WEHI-3 leukemia cells in a dose-dependent manner, and the IC50 for 24-hour treatment was 5.0 mM approximately. The purpose of this study was to evaluate the anti-cancer activity of CCY1a-E2 in syngeneic BALB/c mice bearing murine WEHI-3 cells. To confirm the induction of leukemia animal model, BALB/c mice were administrated intravenously at doses of 5x106, 1x106, and 2x105 WEHI-3 cells, respectively. Leukemia were successfully induced 14-28 days later at the dose of 5x106 and 1x106 cells. To assess the acute and chronic toxicity of CCY1a-E2, BALB/c mice were administrated intravenously with 100mg/kg of CCY1a-E2 for 7 days continuously and then sacrificed at the 7th day or the 28th day. No significant toxicity was observed in the CCY1a-E2 treated mice. To evaluate the anti-cancer activity, BALB/c mice were administrated CCY1a-E2 intravenously (100mg/kg) with 1x106 WEHI-3 cells simultaneously, or 7 days after WEHI-3 cells injection. CCY1a-E2 significantly enhanced survival rate, improved the body weight loss, reduced the enlargement of spleen and lymph nodes, and prevented liver metastases in the WEHI-3 bearing mice. Furthermore, analysis of peripheral blood revealed that the number of leukocytes in the CCY1a-E2 treated leukemia mice were significantly lower than that in leukemia mice without treatment. Taken together, CCY1a-E2 has potentially anticancer activity.?
關聯:
The 19th Joint Annual Conference of Biomedical Sciences (2004)
