论文部分内容阅读
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 effect of magnetic nano-Fe3O4 particles (MNP-Fe3O4) on the apoptosis of HepG2 cells induced by gambogic acid (GA). Methods HepG2 cells were divided into two groups: GA 0.5 μmol / L monotherapy group (A group), GA 0.5 μmol / L and MNP-Fe3O420 μg / ml combination group (B group) and blank control group (C group). The inhibition rate of HepG2 cell proliferation was detected by MTT assay. The apoptosis rate of HepG2 cells was detected by flow cytometry. The expressions of Bcl-2 and Caspase- 3) Protein expression. Results The inhibitory effect of GA on HepG2 cells was dose-dependent. Compared with group C, the apoptotic rate of HepG2 cells, the expression of Caspase-3 protein and the expression of Bcl-2 protein decreased in group A and B (P <0.05), and the changes in group B were more significant (P <0.05). Conclusions MNP-Fe3O4 can enhance the apoptosis-inducing effect of GA on HepG2 cells. The mechanism may be related to the down-regulation of Bcl-2 expression and up-regulation of Caspase-3.