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作 者:鲍世韵[1] 李富荣 郭跃华[3] 桂玲[4] 周汉新
机构地区:[1]430022武汉华中科技大学同济医学院附属协和医院肝胆外科 [2]暨南大学第二临床医学院深圳市人民医院临床医学研究中心 [3]华中科技大学同济医学院附属协和医院肝胆外科 [4]华中科技大学同济医学院药理系
出 处:《中华实验外科杂志》2006年第5期534-536,共3页Chinese Journal of Experimental Surgery
基 金:广东省自然科学基金资助项目(04006966);深圳市科技计划资助项目(2002-K3-121)
摘 要:目的探讨卡铂碳包铁纳米笼壳聚糖微球(C-Fe@CN-CN)对人肝癌细胞株HepG2 增殖和细胞周期的影响。方法应用反相微乳法制备C-Fe@CN-CN,采用噻唑蓝(MTT)法检测不同药物浓度(20、40、80、160 mg/L)的C-Fe@CN-CN对HepG2细胞作用24、48、72 h的生长抑制效应;流式细胞仪分析药物浓度为8、16 mg/L,作用48 h时细胞周期的改变。结果 C-Fe@CN-CN 对人肝癌细胞增殖有明显抑制作用,并呈剂量和时间依赖性。随剂量增加,24 h抑制率由18.8%增至53.2%,随时间延长,抑制率由53.2%增至98.7%。微球作用24 h时抑制效应低于原药,作用48 h 和72 h时抑制效应等同于原药。C-Fe@CN-CN或原药作用48 h后,肝癌细胞周期阻滞于S期 (47.2%),随药物浓度增加,S期阻滞(59.3%)更加明显。空白微球对肝癌细胞增殖和细胞周期分布无影响。结论 C-Fe@CN-CN在体外能有效地抑制肝癌细胞增殖,机制与原药相同,均为诱导S 期阻滞。Objective To investigate the effect of the carboplatin-Fe@C nanocage-loaded chitosan nanoparticles (C-Fe@CN-CN) on the proliferation and cell cycle of human hepatoma cell line HepG2 in vitro. Methods The C-Fe@CN-CN were prepared by the reverse microemulsion method. The inhibitory effect of C-Fe@CN-CN on the proliferation of the HepG2 cell was measured by MTT colorimetry at four levels of drug concentrations(20, 40, 80 and 160 mg/L) in 24, 48 and 72 h. The distribution of cell cycle was analysed by flow cytometry at two levels of drug concentrations (8 and 16 mg/L) in 48 h. Results C-Fe@CN-CN could apparently inhibit the proliferation of HepG2 cell in the dose- and time-dependent manner. With the increase of drug concentration the inhibitory effect was raised from 18.8% to 53.2% in 24 h. With the prolongation of time the inhibitory effect was raised from 53.2% to 98.7%. The inhibitory effect of C-Fe@CN-CN in 24 h was lower than that of original carboplatin, and equal to original carboplatin in 48 h and 72 h. Cell cycle analysis revealed that C-Fe@CN-CN or original carboplatin blocked HepG2 cell in S phase in dose-dependent manner from 47.2% to 59.3% in 48 h. Fe @CN-CN had no effect on the proliferation and cell cycle of HepG2 cell. Conclusion C-Fe@CN-CN can effectively inhibit the proliferation of HepG2 cell through the similar mechanism as original carboplatin indueing the arrest of S phase.
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