OBJECTIVE To examine the effect of uroacitide (CDA-Ⅱ ), an extraction product from normal human urine, on proliferation and differentiation of human glioma SWO-38 cells. METHODS The effects of CDA-Ⅱ on cellular surv...OBJECTIVE To examine the effect of uroacitide (CDA-Ⅱ ), an extraction product from normal human urine, on proliferation and differentiation of human glioma SWO-38 cells. METHODS The effects of CDA-Ⅱ on cellular survival and colony formation were determined by MTT and colony-formation assays. The in vivo anti-tumor effect of CDA-Ⅱ was examined on transplanted SWO-38 cells in nude mice. In addition, the aterations in cell morphology induced by CDA-Ⅱ were observed by H&E staining. RESULTS Treatment of SWO-38 cells with 1-5 mg/ml of CDA-Ⅱ for 3 days, resulted in 39.49% ± 5.27%-65.05% ± 5.89% growth inhibition with an IC50 of 2.52 mg/ml. Based on the colony-formation assay, 10 days of CDA-Ⅱ treatment at a level of 0.3-2.1 mg/ml caused 23.45% ± 0.62%-96.22% ± 1.01% inhibition with an IC50 of 1.03 mg/ml. Furthermore, the inhibitory response was dose-dependent. CDA-Ⅱ at dosage of 500 mg/kg or 2,000 mg/kg per day for 4 weeks significantly suppressed the growth of human glioma SWO 38 cells in nude mice, with inhibition being 47.77% and 79.94%, respectively (P <0.05, n=10). H&E staining and light microscopy revealed that CDA-Ⅱ induced differentiation of the SWO-38 cells. CONCLUSION CDA-Ⅱ has a significant anti-tumor effect on the human glioma SWO-38 cells, and is a potential and natural anti-glioma therapeutic reagent.展开更多
文摘OBJECTIVE To examine the effect of uroacitide (CDA-Ⅱ ), an extraction product from normal human urine, on proliferation and differentiation of human glioma SWO-38 cells. METHODS The effects of CDA-Ⅱ on cellular survival and colony formation were determined by MTT and colony-formation assays. The in vivo anti-tumor effect of CDA-Ⅱ was examined on transplanted SWO-38 cells in nude mice. In addition, the aterations in cell morphology induced by CDA-Ⅱ were observed by H&E staining. RESULTS Treatment of SWO-38 cells with 1-5 mg/ml of CDA-Ⅱ for 3 days, resulted in 39.49% ± 5.27%-65.05% ± 5.89% growth inhibition with an IC50 of 2.52 mg/ml. Based on the colony-formation assay, 10 days of CDA-Ⅱ treatment at a level of 0.3-2.1 mg/ml caused 23.45% ± 0.62%-96.22% ± 1.01% inhibition with an IC50 of 1.03 mg/ml. Furthermore, the inhibitory response was dose-dependent. CDA-Ⅱ at dosage of 500 mg/kg or 2,000 mg/kg per day for 4 weeks significantly suppressed the growth of human glioma SWO 38 cells in nude mice, with inhibition being 47.77% and 79.94%, respectively (P <0.05, n=10). H&E staining and light microscopy revealed that CDA-Ⅱ induced differentiation of the SWO-38 cells. CONCLUSION CDA-Ⅱ has a significant anti-tumor effect on the human glioma SWO-38 cells, and is a potential and natural anti-glioma therapeutic reagent.
