齐墩果酸对HL-60细胞AKT磷酸化的影响  

Effect of oleanolic acid on AKT phosphorylation of HL-60 cells

作　　者：王旭洋 郭丽双[1] 张鹏霞[2] 李红[1] 马微[1] WANG Xu-yang(Mudanjiang Medical University,Mudanjiang 157011,China)

机构地区：[1]牡丹江医学院,黑龙江牡丹江157011 [2]佳木斯大学基础医学院,黑龙江佳木斯154007

出　　处：《牡丹江医学院学报》2021年第2期19-22,共4页Journal of Mudanjiang Medical University

基　　金：牡丹江医学院大学生创新创业项目(201810229012)。

摘　　要：目的研究齐墩果酸(Oleanolic Acid,OA)对人类急性粒细胞性白血病肿瘤细胞HL-60增殖、凋亡的影响及其发挥作用的机制,并分析OA能否抑制PI3K/AKT通路中AKT蛋白的磷酸化。方法以人HL-60细胞作为研究对象,设立对照组与实验组,对照组不加OA,而实验组加入浓度80μmol/L的OA后,利用CCK-8法检测两组细胞增殖情况、流式细胞仪检测细胞凋亡、Western Blot法检测P110α、AKT、p-AKT(Ser473)、p-AKT(Thr308)、mTOR蛋白的表达。结果OA能够抑制HL-60细胞增殖,促进HL-60细胞凋亡,并能下调P110a、p-AKT(Ser473)、p-AKT(Thr308)的表达。结论OA能够抑制HL-60细胞增殖并促进细胞凋亡,并可能通过抑制PI3K/AKT通路中的AKT Ser473及Thr308位点的磷酸化来发挥此作用。Objective To analyze the effect of oleanolic acid(OA)on the proliferation,apoptosis of human acute myeloid leukemia tumor cells HL-60 and its mechanism of action,and to further analyze whether OA can inhibit the phosphorylation of AKT protein in the PI3K/AKT pathway.Methods Human HL-60 cells were used as the research object,and the control group and research group were established.OA drugs at a concentration of 80μM applied to research group while the control group added no OA.The CCK-8 method was used to detect the proliferation of the two groups.Cell apoptosis was detected by flowing cytometry.Western Blotting was used to detect the expression of P110αand AKT,P-AKT(Ser473),p-AKT(Thr308),mTOR protein.Results OA could inhibit the proliferation of HL-60 cells,promote the apoptosis of HL-60 cells,and down-regulate the expression of P110a,p-AKT(Ser473),and p-AKT(Thr308).Conclusion Oleanolic acid can inhibit proliferation and promote apoptosis of HL-60 cell,and may perform this function by inhibiting the phosphorylation of AKT Ser473 and Thr308 in the PI3K/AKT pathway.

关 键 词：齐墩果酸 HL-60 p-AKT(Ser473) p-AKT(Thr308) 磷酸化 

分 类 号：R967[医药卫生—药理学]