EZH2对HSC-T6细胞增殖活化的影响及其部分机制研究

被引:10
作者
陈小霞 [1 ,2 ]
谢娟 [1 ,2 ]
黄成 [1 ,2 ]
孟晓明 [1 ,2 ]
李俊 [1 ,2 ]
机构
[1] 安徽医科大学药学院
[2] 安徽医科大学肝病研究所安徽省高校产业共性技术研究院
基金
安徽省自然科学基金;
关键词
组蛋白甲基化; 肝星状细胞; Zeste基因增强子同源物2; DZNep; 肝纤维化; p-ERK; p-AKT; α平滑肌肌动蛋白;
D O I
暂无
中图分类号
R575.2 [肝硬变];
学科分类号
100201 [内科学];
摘要
目的探讨Zeste基因增强子同源物2(enhancer of zeste homolog 2,EZH2)表达沉默对大鼠肝星状细胞HSC-T6细胞增殖活化的影响,及其部分调控机制。方法应用EZH2的抑制剂DZNep(3-Deazaneplanocin A)作用于TGF-β1诱导活化的HSC-T6细胞,采用Western blot法检测蛋白EZH2、p-ERK、p-AKT和α-SMA的表达;根据EZH2的碱基序列设计并合成小干扰RNA(small interfering RNA,si RNA),通过脂质体LipofectamineTM2000转染到HSC-T6细胞内,应用四甲基偶氮唑盐(MTT)法检测HSC-T6细胞的增殖变化,Western blot法检测蛋白EZH2、p-ERK、p-AKT和α-SMA的表达。结果将DZNep加入TGF-β1诱导活化的HSC-T6细胞后,EZH2蛋白水平明显降低,同时p-ERK、pAKT和α-SMA蛋白水平亦明显降低;将EZH2-si RNA转染活化的HSC-T6细胞内,HSC-T6细胞的增殖可明显被抑制,同时EZH2、p-ERK、p-AKT和α-SMA蛋白水平亦明显降低。结论抑制EZH2的表达可明显抑制HSC-T6细胞的增殖活化,EZH2可能是潜在的治疗肝纤维化的靶点。
引用
收藏
页码:1061 / 1065
页数:5
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