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机构地区:[1]第三军医大学西南医院病理科西南癌症中心,400038 [2]第三军医大学西南医院西南医院肝胆外科,重庆400038
出 处:《实用临床医药杂志》2010年第7期10-14,共5页Journal of Clinical Medicine in Practice
基 金:国家重点基础研究发展计划(973计划)资助项目(2004CB518804)
摘 要:目的探讨不同浓度的阿霉素对肝癌细胞增殖的抑制效果。方法不同浓度阿霉素分别处理肝癌细胞株,采用CCK-8比色分析法检测阿霉素对肝癌细胞增殖的抑制效果,并通过流式细胞仪(FCM)检测阿霉素对肝癌细胞细胞周期分布的影响。结果当阿霉素浓度较低时(小于80 ng/mL),阿霉素对肝癌细胞没有杀伤作用或可在一定程度上刺激肿瘤细胞增殖。当ADM浓度增高至400 ng/mL时对肝癌细胞株HepG2抑制作用最显著,ADM作用96 h后HepG2细胞存活率为(60.4±1.59)%,显著低于Hep3B[(87.89±1.94)%](P<0.01)。流式细胞仪检测细胞周期,结果显示阿霉素处理后Hep3B细胞G1期比例减少发生S期阻滞。结论低浓度的阿霉素可通过诱导细胞周期阻滞而促进肝癌细胞增殖。Objective To investigate the inhibitory effect of different doses of adriamycin (ADM) on the proliferation of human hepatocellular carcinoma (HCC) cell lines. Methods The HCC cell lines were treated with different doses of ADM, the growth rate of cancer cells was analyzed by CCK-8 assay, and the cell cycle distribution was detected by flow cytometry (FCM). Results Our data showed that when the concentration of ADM was low (less than 80 ng/mL), ADM can stimulate the proliferation of tumor ceils to some extent. When HCC ceils were treated with ADM at the dosage of 400 ng/mL, the inhibitory effect on HepG2 cell line was the most significant. After 96 h of treatment with ADM, the viability of HepG2 cells was (60.4 ±1.59% ), which was significantly lower than that of Hep3B (87.89 ±1.94% ), P〈0.01). FCM data demonstrated that administration of ADM could reduced the proportion of G1 phase and resulted in more cells accumulated at S phase in Hep3B cells. Conclution Low concentration of ADM can stimulate the proliferation of Hepatocarcinoma cells through inducing cell cycle arrest.
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