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.
出处
《江苏医药》
CAS
CSCD
北大核心
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)
