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作 者:田彦璋[1] 苗青旺[2] 赵浩亮[1] 李辉宇[1] 贺杰峰[1]
机构地区:[1]山西医科大学第一医院普外科,太原030001 [2]太原市中心医院普外科
出 处:《中国药物与临床》2011年第7期778-779,共2页Chinese Remedies & Clinics
基 金:山西省卫生厅科技攻关项目(200910)
摘 要:目的探讨黄芪甲苷对耐药肝癌细胞株HepG2/GCS多药耐药的逆转作用及可能机制。方法以噻唑蓝(MTT)法测定黄芪甲苷的细胞毒作用和处理前后肝癌细胞对阿霉素的敏感性变化,通过Westernblot法检测细胞GCS蛋白的表达。结果黄芪甲苷在实验浓度范围内对HepG2、HepG2/GCS细胞均无明显毒性;浓度为40μg/ml的黄芪甲苷可逆转HepG2/GCS细胞对阿霉素的耐药性,逆转倍数为1.50,同时细胞内GCS蛋白的表达下降。结论黄芪甲苷具有逆转HepG2/GCS细胞多药耐药的作用,可能与下调细胞内GCS基因表达有关。Objective To explore the role of astragaloside IV in reversing muhidrug resistance of hepatocellular carcinoma cell line HepG2/GCS and its possible mechanisms. Methods MTT assay was used to detect the toxicity of astragaloside 1V and the drug susceptibility change of hepatoma carcinoma cells to doxorubicin (ADM). The expression of GCS protein was analyzed by Western blot. Results Astragaloside IV had no significant cytotoxicity on HepG2 and HepG2/GCS under the test concentration. Astragaloside IV at 40 μg/ml reversed the drug resistance of HepG2/GCS cells to ADM with a reversal index of 1.50, and decreased the expression of GCS protein. Conclusion Astragaloside IV can reverse the muhidrug resistance of HepG2/GCS, which probably is related with its down-regulation of CCS gene expression.
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