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作 者:刘娟[1] 田亮[2] 陈宝安[2] 程坚[2] 夏国华[2] 夏金荣[1] 张海军[2] 张海伟[3] 王雪梅[4]
机构地区:[1]东南大学附属中大医院消化病科,江苏省210009 [2]东南大学附属中大医院血液肿瘤科,江苏省210009 [3]中国药科大学江苏省肿瘤发生与干预重点实验室 [4]东南大学生物科学与医学工程系
出 处:《江苏医药》2012年第12期1379-1381,共3页Jiangsu Medical Journal
基 金:国家973项目资助(2010CB732404);国家自然科学基金(81170492);江苏省医学重点学科资助(2011)
摘 要:目的研究磁性纳米Fe3O4颗粒(MNP-Fe3O4)对藤黄酸(GA)诱导肝癌HepG2细胞凋亡的作用。方法将HepG2细胞分为GA 0.5μmol/L单药组(A组)、GA 0.5μmol/L和MNP-Fe3O420μg/ml两药联合组(B组)及空白对照组(C组)。采用MTT法检测HepG2细胞增殖的抑制率,流式细胞术检测细胞的凋亡率,Western blot法检测B细胞淋巴瘤/白血病2(Bcl-2)及半胱天冬氨酸蛋白酶3(Caspase-3)蛋白的表达。结果 GA对HepG2细胞生长的抑制作用呈剂量依赖性。与C组相比,A、B组HepG2细胞凋亡率、Caspase-3蛋白表达增加,Bcl-2蛋白表达减少(P<0.05),且B组各指标变化更为显著(P<0.05)。结论 MNP-Fe3O4能增强GA对肝癌HepG2细胞的凋亡诱导作用;其机制可能与Bcl-2表达下调及Caspase-3表达上调有关。Objective To investigate the effects of magnetic nanoparticle Fe3O4 (MNP-Fe3O4) on apoptosis of hepatocellular carcinoma HepG2 cells induced by gambogic acid (GA). Methods HepG2 cells were divided into three groups of A (treated with GA 0. 5 μmol/L), B (treated with GA 0. 5 μmol/L plus MNP-Fe3O4 20μg/rnl) and C(blank controls). The inhibitory rate of cell proliferation and the cell apoptosis were analyzed by MTT assay and flow cytometry, respectively. The protein expressions of B cell lymphoma/leukemia-2(Bcl-2) and cystein asparate proteinase-3 (Caspase-3) were detected by Western blot. Results GA had an inhibitory effect on proliferation of HepG2 cells in a dose-dependent manner. Compared with group C, the apoptosis of HepG2 cells and the protein expression of Caspase-3 were increased, while the protein expression of Bcl-2 was decreased in groups of A and B(P〈0. 05), the changes of which were more significant in group B(P〉0. 05). Conclusion MNP-Fe304 can promote GA-induced apoptosis of HepG2 cells, which may be related to down- regulating the expression of Bcl-2 and up-regulating the expression of Caspase-3.
关 键 词:磁性纳米Fe3O4颗粒 藤黄酸 肝癌HEPG2细胞 细胞凋亡
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