18β-甘草次酸对肝癌HepG2细胞增殖及PI3K、PDK1、AKT蛋白表达的影响

发布时间：2018-05-27 22:09

本文选题：肝癌 + 肝癌细胞　；参考：《山东医药》2017年03期

【摘要】：目的观察18β-甘草次酸(18β-GA)对肝癌Hep G2细胞增殖及磷脂酰肌醇-3激酶(PI3K)、磷脂酰肌醇依赖性蛋白激酶1(PDK1)、蛋白激酶B(AKT)蛋白表达的影响。方法 118β-GA对Hep G2细胞增殖的影响观察:以20、40、60、80、100μg/m L的18β-GA作用于Hep G2细胞,分别于培养24、48、72 h后采用MTT法观察细胞增殖情况,以细胞增殖抑制率50%为依据,选择合适的18β-GA作用浓度和作用时间进行后续实验。218β-GA对Hep G2细胞中PI3K、PDK1、AKT蛋白表达的影响观察:将Hep G2分为处理组和对照组,处理组加入40μg/m L的18β-GA,对照组加入等体积的DMSO,培养48 h后采用Western blotting法检测两组细胞中的PI3K、PDK1、AKT蛋白。结果相同18β-GA浓度下,随着作用时间延长,Hep G2细胞增殖抑制率逐渐升高,基本呈时间依赖性;相同作用时间、不同浓度18β-GA作用后细胞增殖抑制率升高,基本呈浓度依赖性。处理组细胞中PI3K、PDK1、AKT蛋白相对表达量分别为0.49±0.08、0.78±0.10、0.84±0.27,对照组分别为0.71±0.11、0.99±0.09、1.88±0.47,两组相比,P均0.05。结论 18β-GA可抑制Hep G2细胞增殖,这种作用可能是通过下调PI3K/AKT通路相关信号分子(PI3K、PDK1、AKT蛋白)表达实现的。
[Abstract]:Objective to investigate the effects of 18 尾 -glycyrrhetinic acid (18 尾 -GAA) on the proliferation and expression of phosphatidylinositol 3 kinase (PI3KK), phosphatidylinositol dependent protein kinase (PI3K1), protein kinase (PKK) in Hep G2 cells. Methods the effect of 118 尾 -GA on the proliferation of Hep G2 cells was observed. The proliferation of Hep G2 cells was observed by MTT assay after cultured for 24 ~ 48 ~ 72 h with 18 尾 -GA at 80100 渭 g / mL. The inhibition rate of cell proliferation was 50%. The effect of 18 尾 -GA on the expression of PI3KnPDK1AK protein in Hep G2 cells was observed by selecting the appropriate concentration and time of treatment. Hep G2 was divided into two groups: treatment group and control group. The treatment group was treated with 40 渭 g / mL 18 尾 -GA and the control group with the same volume of DMSO.After cultured for 48 h, the PI3KnPDK1AKT protein was detected by Western blotting assay. Results at the same concentration of 18 尾 -GA, the inhibitory rate of proliferation of Hep G2 cells increased gradually with the prolongation of time, basically in a time-dependent manner, and the inhibition rate of proliferation of Hep G2 cells increased in a dose-dependent manner after treatment with different concentrations of 18 尾 -GA for the same time. The relative expression of PDK1AKT protein was 0.49 卤0.080.78 卤0.100.84 卤0.27 in the treated group and 0.71 卤0.110.99 卤0.09 卤1.88 卤0.47 in the control group, respectively. Conclusion 18 尾 -GA can inhibit the proliferation of Hep G2 cells, which may be achieved by down-regulating the expression of PI3KnPDK1AK protein, a signal molecule associated with the PI3K/AKT pathway.
【作者单位】：北方民族大学生物科学与工程学院;北京大学医学部;
【基金】：国家民族事务委员会科研项目(12BFZ020) 北方民族大学重点科研项目(2015KJ37) 国家民委生态系统模型及应用重点实验室项目(2012SY01)
【分类号】：R735.7

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