灯盏细辛注射液抗肝癌增殖转移及机制研究  

Study on the anti-proliferative and anti-metastatic effects of Erigeron breviscapus injection on hepatocellular carcinoma and its mechanisms

作　　者：乔旭柏[1] 郭修平 李瑞 王璐璐[2] QIAO Xubai;GUO Xiuping;LI Rui;WANG Lulu(Department of Pathology,Beijing United Family Hospital,Beijing 100015,China;Department of Virology,Institute of Medicinal Biotechnology,Chinese Academy of Medical Sciences&Peking Union Medical College,Beijing 100050,China)

机构地区：[1]北京和睦家医院病理科,100015 [2]中国医学科学院北京协和医学院医药生物技术研究所病毒室,北京100050

出　　处：《中国医药生物技术》2025年第1期80-88,共9页Chinese Medicinal Biotechnology

基　　金：中国医学科学院医学与健康科技创新工程(2022-I2M-1-016,2022-I2M-2-002,2023-I2M-2-006)。

摘　　要：目的探究灯盏细辛注射液(EBI)体内外对肝癌的抗肿瘤作用及线粒体凋亡通路相关机制。方法培养人肝癌细胞系HCCLM3、Huh7和HepG2,采用CCK-8法检测细胞活力,细胞死活染色实验检测细胞死亡情况;通过Transwell迁移实验评估细胞迁移能力;使用Western blot检测线粒体凋亡相关蛋白Bcl-2、Bax和caspase-3的表达变化;构建高转移性的人肝癌细胞HCCLM3皮下移植瘤模型,比较皮下移植瘤生长和肝脏转移情况。结果CCK-8实验显示,EBI以剂量依赖性方式抑制HCCLM3、Huh7和HepG2细胞增殖,IC50值分别为81.41、177.90和209.70μg/mL;细胞死活染色实验结果显示,EBI促进HCCLM3细胞死亡,呈浓度依赖性;Transwell迁移实验显示,EBI处理显著降低细胞迁移数量,呈浓度依赖性。Western blot分析显示,EBI降低抗凋亡蛋白Bcl-2的表达,上调促凋亡蛋白Bax的表达,并降低执行切割的caspase-3前体蛋白的表达,且调控作用呈浓度依赖性,表明EBI激活线粒体凋亡途径。体内实验显示,EBI显著抑制HCCLM3移植瘤的生长及肝脏转移。结论EBI在体内外均能显著抑制肝癌细胞的增殖和转移,其作用机制可能通过激活线粒体凋亡途径实现。Objective To investigate the anti-tumor effects of Erigeron breviscapus injection(EBI)on hepatocellular carcinoma(HCC)both in vitro and in vivo,and to elucidate the underlying mechanisms related to the mitochondrial apoptosis pathway.Methods Human HCC cell lines HCCLM3,Huh7,and HepG2 were cultured and treated with various concentrations of EBI.Cell viability was assessed using the CCK-8 assay,while cell death was evaluated through Calcein AM/PI live/dead staining.The migration ability of the cells was determined using the Transwell migration assay.Western blot analysis was performed to detect the expression levels of mitochondrial apoptosis-related proteins,including Bcl-2,Bax,and caspase-3.An in vivo high-metastatic HCCLM3 subcutaneous xenograft model was established to compare tumor growth and liver metastasis between EBI-treated and control groups.Results The data from CCK-8 assays demonstrated that EBI inhibited the proliferation of HCCLM3,Huh7,and HepG2 cells in a dose-dependent manner,with IC50 values of 81.41,177.90,and 209.70μg/mL,respectively.Live/dead staining results indicated that EBI promoted cell death in HCCLM3 cells in a concentration-dependent manner.EBI also significantly reduced the migration ability of HCC cells in a dose-dependent manner through Transwell migration assays.The results from Western blot analysis showed that EBI decreased the expression of the anti-apoptotic protein Bcl-2,increased the expression of the pro-apoptotic protein Bax,and reduced the expression of the precursor of cleaved caspase-3,suggesting the activation of the mitochondrial apoptosis pathway.Furthermore,EBI significantly inhibited the growth of HCCLM3 xenografts and reduced liver metastasis.Conclusion EBI exhibits significant anti-tumor effects on hepatocellular carcinoma both in vitro and in vivo.The underlying mechanism is likely through the activation of the mitochondrial apoptosis pathway.These findings support the potential of EBI as a novel therapeutic agent for HCC and provide a foundation for future clini

关 键 词：灯盏细辛注射液 肝细胞癌 细胞凋亡 抗肿瘤 

分 类 号：R96[医药卫生—药理学]