摘要
目的研究大黄素增强砷剂的抑瘤作用,探讨肿瘤细胞敏感性、抗凋亡信号NF-κB激活与氧化还原状态的关系。方法在HeLa细胞移植瘤的动物模型上,应用不同剂量大黄素和砷剂腹腔注射,2周后检测瘤重、体重;留取新鲜组织,检测其抗氧化能力;瘤组织分离培养后,用荧光素酶报告基因法和凝胶电泳迁移率分析法,检测NF-κB与DNA结合能力和促进转录能力。结果大黄素增强了砷剂抑制裸鼠移植瘤生长的作用;肿瘤大小与抗氧化能力呈正相关(r=0.826);大黄素能增强砷剂抑制NF-κB结合DNA、促进转录的能力。结论大黄素通过干预肿瘤细胞氧化还原状态,抑制NF-κB结合DNA、促进转录的能力,最终提高砷剂体内抑瘤效果。
ObjectiveTo study whether emodin facilitates the tumor-suppressing efficacy of arsenic trioxide in tumor-bearing mice,and to explore the relation of susceptibility of tumor cells with apoptosis, transactivation of anti-apoptic signal NF-B, and cellular redox state.MethodsThe tumor-bearing mice with Hela cells were intraperitoneally administered with emodin and arsenic trioxide alone or both in different doses for 2 weeks, and then sacrificed for measurement of body weight and tumor weight. The tumor tissues were freshly assessed for anti-oxidation capacity. The tumor cells were subcultured and evaluated for NF-B binding capacity to DNA with electrophoretic mobility shift assay, and NF-B transactivation with luciferase assay.ResultsEmodin facilitated the tumor-suppressing efficacy of arsenic trioxide in tumor-bearing mice. The tumor weight was positively correlated with its anti-oxidation capacity((r=0.826).) Emodin enhanced the effect of arsenic trioxide on inhibition of NF-B binding capacity to DNA and NF-B transactivation.ConclusionEmodin facilitates the tumor-suppressing efficacy of arsenic trioxide in tumor-bearing mice in vivo via interfering cellular redox state and inhibition of NF-B binding capacity to DNA and NF-B transactivation.
出处
《上海第二医科大学学报》
CSCD
北大核心
2005年第7期666-670,共5页
Acta Universitatis Medicinalis Secondae Shanghai
基金
国家自然科学基金(30170475)资助项目.
