番荔素纳米混悬剂的制备及其抗肿瘤作用研究

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目的制备高载药量番荔素纳米混悬剂(ACGs-NSPs),并研究其对小鼠乳腺癌4T1移植肿瘤的生长抑制作用,为强效抗肿瘤药物ACGs的临床应用提供可用注射剂型。方法番荔素、TPGS、SPC(质量比7:5:2)采用超声-沉淀法制备ACGs-NSPs,并用动态光散射法测定ACGs-NSPs的粒径,透射电镜观察其形态;稳定剂TPGS、SPC组成比例对ACGs-NSPs的溶血性考察;透析法考察其体外释放;采用MTT比色法评价ACGs-NSPs对4T1细胞细胞毒性;建立4T1乳腺癌皮下小鼠肿瘤模型,以紫杉醇注射液(PTX)为阳性对照,考察不同剂量ACGs-NSps静脉注射给药对4T1肿瘤的抗肿瘤药效。结果ACGs-NSPs为表面光滑的球形,平均粒径为(129.03±1.03)nm,多分散指数PDI为0.134±0.03,zeta为(-17.7±0.16)m V,HPLC法测得番荔素线性回归方程为Y=0.157 2 X-0.363 2(R2=0.999),在5~200μg/m L范围内显性关系良好,载药量高达(45.03±0.72)%;体外释放较为缓慢;MTT试验中,ACGs-NSPs对4T1乳腺癌的细胞毒性显著强于游离药物(IC50,3.221μg/m L vs 4.464μg/m L,P<0.05);4T1荷瘤小鼠的药效学实验中,ACGs-NSPs表现出剂量相关性的抑瘤作用,高、中、低剂量组(0.4、0.2、0.1 mg/kg)抑瘤率分别为76.09%、74.34%、42.03%;但高剂量组小鼠有死亡(3/10)。结论成功制备高载药量的ACGs-NSPs,且其对4T1乳腺癌有显著的抑制作用;从药效和小鼠存活率来看,0.2 mg/kg为合适的给药剂量。 OBJECTIVE To prepare ACGs-NSPs with high drug loading capacity and to study their inhibitory effect on the growth of 4T1-transplanted breast cancer in mice and to provide a ready-to-use injection for the clinical application of potent antitumor agents ACGs. Methods ACGs-NSPs were prepared by ultrasound-precipitation method and the particle size of ACGs-NSPs was determined by dynamic light scattering. The morphologies of ACGs-NSPs were observed by transmission electron microscopy. The stability of TPG, TPGS and SPC (mass ratio 7: SPC ratio of ACGs-NSPs hemolytic study; Dialysis method in vitro release; MTT colorimetric evaluation of ACGs-NSPs on 4T1 cells cytotoxicity; 4T1 breast cancer subcutaneous mouse tumor model established with paclitaxel injection (PTX ) As a positive control, to investigate different doses of ACGs-NSps intravenous injection of 4T1 tumor anti-tumor efficacy. Results The average diameter of ACGs-NSPs was (129.03 ± 1.03) nm with a polydispersity index of 0.134 ± 0.03 and a zeta of (-17.7 ± 0.16) mV. The linear regression of diclofin The equation was Y = 0.157 2 X-0.363 2 (R2 = 0.999), with a dominant relationship in the range of 5 ~ 200 μg / mL. The drug loading was as high as (45.03 ± 0.72)% and the release in vitro was slow. In the MTT assay, The cytotoxicity of ACGs-NSPs to 4T1 breast cancer was significantly higher than that of free drug (IC50, 3.21 1μg / m L vs 4.464μg / m L, P <0.05). In the pharmacodynamic experiments of 4T1 tumor-bearing mice, ACGs-NSPs (0.4,0.2,0.1 mg / kg) were 76.09%, 74.34% and 42.03%, respectively; however, the mice in the high dose group died 3/10). CONCLUSIONS: ACGs-NSPs with high drug loadings were successfully prepared and had a significant inhibitory effect on 4T1 breast cancer. In terms of efficacy and survival rate of mice, 0.2 mg / kg was the appropriate dosage.
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