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目的探讨松油烯-4-醇(T4O)对人多发性骨髓瘤U266细胞增殖及凋亡的影响及其作用机制。方法不同浓度(5~80μmol/L)T4O体外作用于U266细胞。CCK-8法检测增殖抑制率;AO/EB染色,倒置显微镜观察细胞凋亡形态;比色法检测Caspase-3酶活性;流式细胞术检测细胞凋亡及周期;JC-1染色检测细胞线粒体膜电位。结果 T4O对U266细胞有增殖抑制作用,呈时间-剂量依赖性(P<0.05)。T4O诱导U266细胞凋亡,呈剂量依赖性(P<0.05),随药物浓度增加,Caspase-3酶活性逐渐增强(P<0.05),线粒体膜电位逐渐降低(P<0.05),细胞周期被阻滞在G2期。结论 T4O对U266细胞有抑制增殖及促凋亡作用,其机制是激活细胞凋亡途径关键酶Caspase-3,使细胞线粒体膜电位降低,并且使细胞周期阻滞在G2期,进而抑制肿瘤细胞分化与增殖。
Objective To investigate the effect of terpinen-4-ol (T4O) on the proliferation and apoptosis of human multiple myeloma U266 cells and its mechanism. Methods U266 cells were treated with different concentrations of T4O (5 ~ 80μmol / L) in vitro. CCK-8 method was used to detect the proliferation inhibition rate; AO / EB staining and inverted microscope were used to observe the morphological changes of apoptosis; Caspase-3 activity was detected by colorimetric assay; apoptosis and cycle were detected by flow cytometry; Membrane potential. Results T4O inhibited proliferation of U266 cells in a time-and dose-dependent manner (P <0.05). T4O could induce the apoptosis of U266 cells in a dose-dependent manner (P <0.05). With the increase of drug concentration, the activity of Caspase-3 gradually increased (P <0.05) and the mitochondrial membrane potential decreased (P <0.05) Lag in G2 period. Conclusion T4O can inhibit proliferation and induce apoptosis of U266 cells by activating Caspase-3, a key enzyme in the apoptosis pathway, decreasing the mitochondrial membrane potential and arresting the cell cycle in G2 phase, which in turn inhibits tumor cell differentiation With proliferation.