注射用核糖核酸Ⅱ通过活性氧介导的PI3K/Akt信号通路诱导人白血病细胞KG1a凋亡

Ribonucleic acid Ⅱ induces apoptosis of human leukemia KG1a cells through PI3K/Akt activation mediated by reactive oxygen

目的 研究注射用核糖核酸Ⅱ诱导人急性骨髓白血病细胞系KG1a细胞凋亡与PI3K/Akt信号通路和活性氧(ROS)的关系。方法 流式细胞术(FCM)检测细胞周期和细胞内的ROS水平;免疫印迹法(Western blot)检测PI3K/Akt信号通路相关蛋白p-PI3K、p-Akt、p-MDM2、p21和周期相关蛋白cyclin D1、CDK4的表达;加入抗氧化剂N-乙酰半胱氨酸(NAC)后,检测p-PI3K、p-Akt和p53蛋白表达变化。结果 FCM结果显示,注射用核糖核酸Ⅱ可将KG1a细胞阻滞在G 0/G 1期,且ROS介导了细胞周期的阻滞;FCM检测ROS结果显示,KG1a细胞内ROS水平均随药物浓度增加而升高;Western blot结果显示,注射用核糖核酸Ⅱ下调p-PI3K、p-Akt、p-MDM2和cyclin D1、CDK4的表达,上调p21的表达;与仅用注射用核糖核酸Ⅱ相比,经NAC预处理后再使用注射用核糖核酸Ⅱ,明显上调了磷酸化PI3K和Akt的表达,下调了p53的表达。结论 注射用核糖核酸Ⅱ通过ROS介导的PI3K/Akt信号通路,诱导人急性骨髓白血病细胞系KG1a细胞凋亡。

Aim To investigate the correlation between ribonucleic acid Ⅱ on human leukemia cell lines KG1a and PI3K/Akt signaling pathway by reactive oxygen.Methods The cell cycle and the ROS level of ribonucleic acid Ⅱ in human leukemia cell lines were determined by flow cytometry.The levels of p-PI3K,p-Akt,p-MDM2,p21,cyclin D1 and CDK4 were detected by Western blot.The expression levels of protein p-PI3K,p-Akt and p53 after treated with ribonucleic acid Ⅱ and NAC were also detected by Western blot.Results The results of FCM revealed that the cell cycle was arrested at G 0/G 1 phase and ROS prevented the arrest of cell cycle.The results also showed that ROS level increased with the concentration of ribonucleic acid Ⅱ in KG1a cells.Western blot results showed after treated with ribonucleic acid Ⅱ,the expression levels of p-PI3K,p-Akt,p-MDM2,cyclin D1 and CDK4 decreased,while p21 increased in KG1a cells.After treated with ribonucleic acid Ⅱ and NAC,the expression levels of p-PI3K and p-Akt increased,while p53 decreased.Conclusion Ribonucleic acid Ⅱ can induce the apoptosis of leukemia KG1a cells through ROS-mediated PI3K/Akt signaling pathway.