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白藜芦醇对人急性T淋巴细胞白血病的体外治疗作用及其机制 被引量:3

Therapeutic effect and mechanism of resveratrol on human T lymphatic leukemia cells
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摘要 目的探讨白藜芦醇对人急性T淋巴细胞白血病的体外治疗作用及其机制。方法以人T淋巴细胞白血病细胞(Hut78)作为白藜芦醇的作用靶细胞,分别用6.25、12.5、25、50、100、200μmol/L白藜芦醇处理Hut78细胞24 h,用100μmol/L白藜芦醇处理Hut78细胞12、24、48 h,采用CCK-8法测算细胞抑制率。经100、200μmol/L白藜芦醇分别处理Hut78细胞12、24 h后,用流式细胞术分析Hut78细胞的凋亡情况。Hut78细胞经100、200μmol/L白藜芦醇处理48 h,采用Western blotting法检测细胞中C-myc蛋白的表达。结果白藜芦醇在大于6.25μmol/L时显著抑制Hut78细胞的增殖,并呈剂量-时间依赖性(P均<0.01)。白藜芦醇可诱导Hut78细胞凋亡,随浓度增加凋亡细胞增多(P均<0.01)。白藜芦醇可呈剂量依赖性下调C-myc蛋白表达(P均<0.01)。结论白藜芦醇有明显的体外抗人急性T淋巴细胞白血病效应,其作用机制可能与下调C-myc蛋白表达有关。 Objective To investigate the therapeutic effect and mechanism of resveratrol( Res) on human T lymphatic leukemia cells( Hut78). Methods Human T lymphocytic leukemia( Hut78) cells were selected as the target cells,which were treated with 6. 25,12. 5,25,50,100 and 200 μmol / L Res,respectively. CCK-8 assay was used to detect the cell inhibition rate of Hut78 cells which were treated with 100 μmol / L Res for 12,24 and 48 h,respectively. Flow cytometry was used to detect the apoptosis of Hut78 cells which were respectively treated with 100 and 200 μmol / L Res for 12 and 24 h. Western blotting was used to detect the expression of C-myc protein in Hut78 cells which were respectively treated with 100 and 200 μmol / L Res for 48 h.Results Resveratrol whose dose was greater than 6. 25 μmol / L significantly inhibited the proliferation of Hut78 cells,and was time- and dose-dependent( all P〈0. 01). Res induced the apoptosis of Hut 78 cells,which was dose-dependent( all P〈0. 01).Res own-regulated the expression of C-myc protein which was in a dose-dependent manner( all P〈0. 01). Conclusion Resveratrol has significant anti-leukemia effect on human T lymphatic leukemia,and its mechanism may be associated with the downregulated expression of C-myc protein.
出处 《山东医药》 CAS 北大核心 2016年第29期1-3,共3页 Shandong Medical Journal
基金 国家自然科学基金资助项目(81070445) 河南省医学科技攻关项目(20090349)
关键词 T淋巴细胞白血病 白藜芦醇 细胞增殖 细胞凋亡 C-MYC蛋白 T lymphatic leukemia resveratrol cell proliferation apoptosis C-myc protein
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