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机构地区:[1]福建医科大学药学院,福州350122 [2]福建医科大学免疫治疗研究所,福州350122
出 处:《福建医科大学学报》2017年第3期146-149,165,共5页Journal of Fujian Medical University
基 金:福建省自然科学基金(2017J01824);福建医科大学苗圃基金(2015MP009)
摘 要:目的观察雷公藤内酯醇(TPL)对肝癌H22细胞增殖、凋亡及环氧合酶-2(COX-2)表达水平的影响。方法以体外培养的鼠源性H22细胞株为研究对象,实验分对照组和不同浓度的TPL处理组。MTT比色法测定TPL对H22细胞株增殖抑制情况;TPL处理48h后,Annexin V-FITC/PI双标记流式细胞术检测细胞凋亡情况,流式细胞术间接免疫荧光双标记法检测COX-2表达变化情况。结果随着药物浓度的增加及时间的延长,TPL能明显抑制H22细胞增殖。TPL诱导细胞凋亡及下调COX-2的表达具有浓度依赖性,不同浓度组比较,差别具有统计学意义(P<0.05)。结论 TPL可能通过诱导肝癌H22细胞凋亡及抑制COX-2表达发挥抗肿瘤作用。Objective To investigate the effects of triptolide(TPL)on proliferation,apoptosis,and cycloxygenase-2(COX-2)expression in liver cancer line H22 and explore its anti-tumor mechanism.Methods H22 cultured in vitro was treated with different concentrations of triptolide,cell proliferation activity was determined by MTT assay. The Annexin V-FITC/PI cell apoptosis and COX-2expression were assessed at 48 hafter the onset of drug treatment by flow cytometry. Result Triptolide significantly inhibited the proliferation of H22 cells in a dose-and time-dependent manner. In addition,triptolide significantly induced cell apoptosis and down-regulated COX-2expression in a dose-manner during48 h. Conclusion TPL may play an anti-liver cancer role by inducing cell apoptosis and inhibiting COX-2expression in H22 cells.
关 键 词:雷公藤内酯 肝肿瘤 细胞凋亡 前列腺素内过氧化物合酶类
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