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作 者:朱晓琴[1] 周于婷[2] 陈新美[3] 肖顺华[3] 赵青[3]
机构地区:[1]广州医学院生理学教研室,广州510182 [2]南方医科大学生物技术学院2008级本科生,广州510515 [3]广州医学院生物化学教研室,广州510182
出 处:《华中科技大学学报(医学版)》2010年第3期376-380,共5页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:广州市教育局市属高校科技计划项目(No.61057,08A112);教育部留学回国人员科研启动基金资助项目(No.教外司留2007-1108号);广州市科技计划项目(No.2009J1-C361);广州市留学回国人员科研启动基金(No.2007-583);广州医学院科研基金(No.2006GD052,2008A08)
摘 要:目的探讨激活大麻受体对肝癌细胞增殖和凋亡的作用,并对其机制进行初步研究。方法将HepG2细胞分成对照组、不同剂量大麻受体激动剂delta9-tetrahydrocannabinol(THC)处理组。MTT法测定THC对HepG2细胞增殖的影响;DNA梯度电泳法和流式细胞仪检测分析各组细胞凋亡情况;Westernblot法分析细胞大麻受体CB1、CB2、Caspase3和c-myc的蛋白表达;分光光度法检测Caspase3的活性。结果 HepG2细胞大麻受体CB1、CB2表达较L02正常肝细胞增高。THC能抑制HepG2细胞增殖,诱导HepG2细胞凋亡,上述效应具有剂量依赖性。THC可抑制HepG2细胞c-myc的表达,诱导HepG2细胞Caspase3的蛋白表达和活性。结论大麻受体激动剂THC能抑制肝癌细胞增殖,诱导肝癌细胞凋亡,此效应可能与其影响c-myc的表达和Caspase3的活性相关。Objective To study the effect and the preliminary mechanism of the activation of cannabinoid receptor by THC on proliferation and apoptosis of hepatoma HepG2 cells.Methods HepG2 cells were divided into control group and THC-treat-ed group treated with different doses of delta9-tetrahydrocannabinol(THC).MTT was used to measure the effects of THC on HepG2 cells.DNA fragmentation and flow cytometry(FCM)were used to examine the effects of THC on the apoptosis of HepG2 cells.CB1/2,cleaved Caspase 3 and c-myc were detected by Western blot,and Caspase 3 activity by colorimetric method.Results The levels of CB1/2 receptors were higher in HepG2 cells than in L02 control cells.THC inhibited HepG2 cell proliferation and induced cell apoptosis dose-dependently.THC inhibited c-myc level,increased Caspase 3 protein levels and Caspase 3 activity.Conclusion THC can inhibit the proliferation and induce the apoptosis of hepatocellular carcinoma cells probably by up-regulating the expression of Caspase 3 protein and down-regulating the expression of c-myc protein.
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