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作 者:熊暮珺 黄靓[2] XIONG Mujun;HUANG Liang(Chenzhou First People's Hospital,Chenzhou Hunan China 423000;The First Affiliated Hospital of Zhongshan University,Guangzhou Guangdong China 510080)
机构地区:[1]郴州市第一人民医院,湖南郴州423000 [2]中山大学附属第一医院,广东广州510080
出 处:《中医学报》2020年第7期1497-1500,共4页Acta Chinese Medicine
基 金:湖南省自然科学基金项目(2018JJ2603)。
摘 要:目的:探讨人参皂苷Rg3对急性髓细胞性白血病的干预机制。方法:体外培养急性单核细胞性白血病细胞系(THP-1)、急髓白血病M3细胞系(HL-60),采用人参皂苷Rg3对细胞系进行干预,采用MTS法检测细胞增殖,流式细胞仪检测细胞凋亡,Western blot法分析相关蛋白表达。结果:人参皂苷Rg3对THP-1、HL-60细胞均有不同程度的抑制生长效果,IC50分别为3.5、3.02 g·L^-1。人参皂苷Rg3作用24 h、48 h均可抑制急性髓细胞性白血病细胞增殖,且抑制作用与药物剂量呈依赖关系;人参皂苷Rg3对THP-1以及HL-60细胞的凋亡可起到诱导作用,细胞凋亡会随药物浓度升高而增加,且干预时间延长同样会增加细胞凋亡率,细胞凋亡率呈现时间、剂量依赖性。在作用48 h后,凋亡相关因子PARP出现了降解分裂条带,THP-1出现了Caspase-8条带轻度减弱,HL-60细胞出现了p-Akt明显减弱。结论:人参皂苷Rg3可以对Caspase-8及PARP相关蛋白的表达以及凋亡过程起到激活作用,使p-Akt表达水平降低,从而对肿瘤细胞的增殖以及凋亡起到抑制以及诱导作用。Objective:To investigate the intervention mechanism of ginsenoside Rg3 on acute myeloid leukemia.Methods:Acute monocytic leukemia cell line(THP-1)and acute myeloid leukemia cell line(HL-60)were cultured in vitro.Ginsenoside Rg3 was used to intervene the cell line.Cell proliferation was detected by MTS method,apoptosis was detected by flow cytometry,and protein expression was analyzed by Western blot.Results:Ginsenoside Rg3 can inhibit the growth of THP-1 and HL-60 cells in varying degrees,with IC50 of 3.5 and 3.02 g·L^-1,respectively;ginsenoside Rg3 could inhibit the proliferation of AML cells in 24 and 48 hours,and the inhibition was dose-dependent;ginsenoside Rg3 can induce the apoptosis of THP-1 and HL-60 cells.The apoptosis will increase with the increase of drug concentration,and the longer intervention time will also increase the apoptosis rate,which is time-dependent and dose-dependent.After 48 hours of treatment,the apoptotic related factor PARP appeared degradation division band,THP-1 appeared caspase 8 band slightly weakened,HL-60 cells appeared p-Akt significantly weakened.Conclusion:Ginsenoside Rg3 can activate the expression of caspase 8 and PARP related proteins and the process of apoptosis,reduce the expression level of p-Akt,thus inhibit and induce the proliferation and apoptosis of tumor cells.
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