异鼠李素通过下调Notch1通路抑制HepG2细胞的增殖并诱导其凋亡  

Isorhamnetin inhibits the proliferation of HepG2 cells by downregulating the Notch1 pathway and induces apoptosis

作　　者：段仁鹏 DUAN Ren-peng(Department of the First Surgical Ward of Minhang Campus,Guangdong Second Provincial General Hospital,Guangzhou 510317,China)

机构地区：[1]广东省第二人民医院民航院区外一科,广州510317

出　　处：《中国处方药》2024年第2期76-79,共4页Journal of China Prescription Drug

摘　　要：目的探究异鼠李素(Isorhamnetin,ISO)是否通过下调Notch1的表达来抑制肝癌HepG2细胞增殖并促进其凋亡。方法使用细胞毒性实验噻唑蓝(MTT)法检测评估HepG2细胞存活率,并使用流式细胞仪分析细胞的凋亡水平。克隆形成实验反应不同异鼠李素浓度下HepG2细胞的增殖情况。采用Western blot测定P53、Bcl-2和Bax的表达情况。结果处理ISO后,HepG2细胞的存活能力表现出明显的剂量和时间依赖性抑制。在ISO处理24 h后,HepG2细胞系中诱导了凋亡。ISO处理以及敲除Notch1蛋白后,上调抑癌基因P53的表达,上调细胞凋亡相关蛋白Bax的表达以及下调Bcl-2的表达。进一步实验发现,Notch1 siRNA可以增强ISO的抗肿瘤特性。结论ISO通过下调Notch1通路抑制肝细胞癌(HCC)细胞的增殖并促进其凋亡。Objective To investigate whether Isorhamnetin ISO downregulates Notch1 expression to inhibit cell proliferation and promote apoptosis.Methods The cytotoxicity assay(MTT assay)was used to evaluate the viability of HepG2 cells,and flow cytometry was employed to analyze the apoptosis level of the cells.The colony formation assay was performed to assess the proliferation of HepG2 cells under different concentrations of paclitaxel.In addition,Western blot analysis was conducted to determine the expression levels of P53,Bcl-2,and Bax.Results Treatment with ISO significantly suppressed the survival of HCC cells in a dose-and time-dependent manner.Induction of apoptosis was observed in HepG2 cell line 24 hours after ISO treatment.Knockdown of Notch1 expression and upregulation of the anti-cancer gene P53 expression were observed after ISO treatment,as well as upregulation of apoptosis-related protein Bax expression and downregulation of Bcl-2 expression.Further experiments showed that Notch1 siRNA enhanced the anti-tumor properties of ISO.Conclusion ISO inhibits the proliferation of HCC cells and promotes apoptosis by downregulating the Notch1 pathway.

关 键 词：异鼠李素 HEPG2细胞 NOTCH1 凋亡 

分 类 号：R965[医药卫生—药理学]