异芒果苷通过调节PTEN-PI3K-AKt-mTOR通路抑制恶性胶质瘤的恶性行为  

Isomangiferin Inhibits Glioblastoma through Regulating PTEN-PI3K-AKt-mTOR Pathway

作　　者：唐春花 宁志丰 周雄飞[3] 毛开新[3] 胡美纯 吴喆 王龙 苏延停 刘星吟 TANG Chunhua;NING Zhifeng;ZHOU Xiongfei;MAO Kaixin;HU Meichun;WU Zhe;WANG Long;SU Yanting;LIU Xingyin(Second Affiliated Hospital of Hubei University of Science and Technology,Xianning 437100,China;School of Basic Medicine Hubei University of Science and Technology,Xianning 437100,China;National Experimental Teaching Demonstration Center of General Medicine Hubei University of Science and Technology,Xianning 437100,China)

机构地区：[1]湖北科技学院附属第二医院,湖北咸宁437100 [2]湖北科技学院基础医学院,湖北咸宁437100 [3]湖北科技学院国家级全科医学实验教学示范中心,湖北咸宁437100

出　　处：《云南中医学院学报》2022年第1期65-71,共7页Journal of Yunnan University of Traditional Chinese Medicine

基　　金：湖北科技学院专项基金(2020LCZ003)。

摘　　要：目的 探索异芒果苷对恶性胶质瘤细胞U251的抑制作用及可能机制。方法 常规培养U251细胞,以一定浓度梯度的异芒果苷与U251细胞共孵育,MTT法检测细胞增殖能力,平板克隆形成实验检测集落形成能力,Transwell小室迁移和侵袭实验检测纵向迁移能力,划痕实验检测横向迁移能力,western blot实验检测PTENPI3K-AKt-mTOR通路的变化,PTEN-siRNA予以验证。结果 与一定浓度梯度的异芒果苷共孵育后,MTT法检测发现U251细胞的增殖能力以时间依赖性和浓度依赖性下降,平板克隆形成实验检测发现U251细胞的集落形成能力浓度依赖性下降,Transwell小室迁移和侵袭实验检测发现U251细胞的纵向迁移和侵袭能力浓度依赖性下降,划痕实验发现U251细胞的横向迁移能力浓度依赖性下降,免疫印迹检测发现,PTEN表达呈浓度依赖性上调,而磷酸化的PI3K、磷酸化的AKt及磷酸化的mTOR呈浓度依赖性下降。PTEN-siRNA沉默PTEN可抵消异芒果苷的抑制作用。结论 异芒果苷可以抑制恶性胶质瘤U251细胞的恶性生物学行为,作用机制与调控PTEN-PI3K-AKtmTOR通路有关。Objective To explore the action and possible mechanism of isomangiferin suppression to malignant glioma cells U251.Method U251 cells were cultivated routinely and then treated with bergenin.Next,the cells were detected by MTT assay to test the viability,plate clone formation assay to test colony formation ability,transwell small chamber migration and invasion assay to test longitudinal migration and invasion ability,scratch healing assay to test lateral migration ability,and western blot to test the change of PTEN-PI3K-AKT-mTOR pathway.Results After the cells treated with certain concentrate gradient isomangiferin,the U251 cell viability declined in a time and concentration dependent way by MTT assay,the colony formation ability of U251 cells was suppressed in a concentration dependent manner by plate clone formation assay,the longitudinal invasion and migration ability were inhibited in a concentration dependent manner through transwell chamber migration and invasion assay,and simultaneously the lateral migration ability was also restrained in same way.Subsequent western blot assay found the expression of PTEN was upregulated,but the phosphorylated PI3K,AKT and mTOR expression quantity declined in a concentration dependent way.Conclusion Isomangiferin can inhibit the malignant biological behavior of malignant glioma cells and the mechanism have relation with regulating PTEN-PI3K-AKTmTOR pathway.

关 键 词：神经胶质瘤 U251细胞 异芒果苷 PTEN-PI3K-AKt-mTOR通路 

分 类 号：R285.5[医药卫生—中药学]