人参皂苷rg5通过调节PI3K信号通路抑制急性白血病细胞的生长  

Ginsenoside rg5 inhibits growth of acute leukemia cells by regulating PI3K signaling pathway

作　　者：桂长清 许力 马娜 Gui Changqing;Xu Li;Ma Na(School of Medicine,Anhui University of Science and Technology,Huainan,Anhui 232001,China;Department of Hematology,the Second People’s Hospital of Anhui Province,Hefei,Anhui 230022,China;Department of CT,Anhui No.2 Provincial People's Hospital,Hefei 230022,China)

机构地区：[1]安徽理工大学医学院,安徽淮南232001 [2]安徽省第二人民医院血液内科,安徽合肥230022 [3]安徽省第二人民医院CT室,安徽合肥230022

出　　处：《齐齐哈尔医学院学报》2025年第4期317-320,共4页Journal of Qiqihar Medical University

基　　金：安徽省高校自然科学研究项目(2023AH053386);安徽省高校自然科学研究项目(K J2019A1107)。

摘　　要：目的 探讨人参皂苷rg5(G-rg5)抗T细胞急性淋巴细胞白血病CCRF-CEM细胞的作用及机制。方法 采用CCK8法检测不同浓度G-rg5对CCRF-CEM细胞的增殖抑制作用,采用流式细胞术分析G-rg5对CCRF-CEM细胞的细胞凋亡的影响;通过Western blot检测G-rg5对CCRF-CEM细胞PI3K/AKT/mTOR信号通路蛋白的表达。结果 CCK-8增殖试验显示,细胞活力随着G-rg5浓度的增高而降低。细胞凋亡率随着用药浓度的增加而增加。G-rg5处理的CCRF-CEM细胞P-PI3K、P-AKT、P-mTOR蛋白表达显著降低,BCL-2下调明显,BAX上调,Bcl-2/BAX比值下降,而非磷酸化的PI3K、AKT和mTOR蛋白未发现显著变化。结论 研究表明,G-rg5可以抑制ALL细胞的增殖,诱导细胞凋亡,这可能受到PI3K信号通路的调控。G-rg5可能是临床ALL治疗的潜在药物。Objective To investigate the role and mechanism of ginsenoside rg5(G-rg5)in inhibiting the proliferation of T-cell acute lymphoblastic leukemia CCRF-CEM cells.Methods In this study,the proliferation inhibitory effect of different concentrations of ginsenoside rg5 on CCRF-CEM cells was detected by CCK8 assay,and the effect of ginsenoside rg5 on apoptosis of CCRF-CEM cells was analyzed by flow cytometry.The effect of ginsenoside rg5 on the PI3K/AKT/mTOR signaling pathway protein expression in CCRF-CEM cells was detected by Western blot.Results CCK-8 proliferation assay showed that cell viability decreased with increasing concentrations of ginsenoside rg5.Apoptosis rate increased with increasing concentration of the drug.Ginsenoside rg5-treated CCRF-CEM cells showed a significant decrease in the expression of P-PI3K,P-AKT,and P-mTOR proteins,a significant down-regulation of BCL-2,an up-regulation of BAX,and a decrease in the Bcl-2/BAX ratio,whereas no significant changes in non-phosphorylated PI3K,AKT,and mTOR proteins were found.Conclusions The present study demonstrated that G-rg5 inhibited proliferation and induced apoptosis in ALL cells,which may be regulated by the PI3K signaling pathway.These results suggest that G-rg5 may be a potential drug for clinical ALL treatment.

关 键 词：CCRF-CEM细胞 人参皂苷-Rg5 凋亡 PI3K/AKT/mTOR通路 

分 类 号：R285.5[医药卫生—中药学]