Ginkgo biloba extract EGb761 conveys an anticancer effect, but little is known regarding its role in hepatocellular carcinoma (HCC). Our study aims to determine the anticancer effect of EGb761 on HCC cell lines and clarify the underlying molecular mechanism. We explore biological functions of EGb761 in HCC using morphological observation, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cytotoxic analysis. We investigate the effects of EGb761 on proliferation and apoptosis of HCC cells using plate clone formation, proliferating cell nuclear antigen, and terminal deoxynucleotidyl transferase d-untranslated protein nick end labeling assays. Protein expressions of the NF-κB/p53 signal pathway were detected and identified using immunohistochemistry. The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-α, an inhibitor of p53. We determine that EGb761 inhibits cell growth, reduces cell viability, and promotes apoptosis of HCC cells. In addition, EGb761 reduces proliferation and increases apoptosis of human hepatocellular carcinomas (HepG2) cells in a dose-dependent manner. We also find that EGb761 exerts an anticancer effect on HepG2 cells by activating p53 and inhibiting nuclear factor (NF)-κB signaling pathways. This study confirms that EGb761 inhibits proliferation and triggers apoptosis of HCC cells through the NF-κB/p53 signaling pathway.

中文翻译：

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银杏叶提取物机制通过核因子-κB/ p53信号通路抑制肝癌。

银杏叶提取物EGb761具有抗癌作用，但对其在肝细胞癌（HCC）中的作用知之甚少。我们的研究旨在确定EGb761对HCC细胞系的抗癌作用，并阐明其潜在的分子机制。我们使用形态学观察，3-（4,5-二甲基噻唑-2-基）-2,5-溴二苯基四唑溴化物（MTT）分析和细胞毒性分析探索EGb761在肝癌中的生物学功能。我们使用板克隆形成，增殖细胞核抗原和末端脱氧核苷酸转移酶d-非翻译蛋白缺口末端标记法研究了EGb761对HCC细胞增殖和凋亡的影响。使用免疫组织化学检测并鉴定了NF-κB/ p53信号通路的蛋白表达。通过添加p53抑制剂pifithrin（PFT）-α，进一步证实了EGb761对p53信号通路的作用。我们确定EGb761抑制细胞生长，降低细胞活力，并促进HCC细胞凋亡。另外，EGb761以剂量依赖性方式减少人肝细胞癌（HepG2）细胞的增殖并增加其凋亡。我们还发现，EGb761通过激活p53和抑制核因子（NF）-κB信号通路，对HepG2细胞发挥抗癌作用。这项研究证实，EGb761通过NF-κB/ p53信号通路抑制增殖并触发HCC细胞凋亡。EGb761以剂量依赖的方式降低人肝癌（HepG2）细胞的增殖并增加其凋亡。我们还发现，EGb761通过激活p53和抑制核因子（NF）-κB信号通路，对HepG2细胞发挥抗癌作用。这项研究证实，EGb761通过NF-κB/ p53信号通路抑制增殖并触发HCC细胞凋亡。EGb761以剂量依赖性方式减少人肝癌（HepG2）细胞的增殖并增加其凋亡。我们还发现，EGb761通过激活p53和抑制核因子（NF）-κB信号通路，对HepG2细胞发挥抗癌作用。这项研究证实，EGb761通过NF-κB/ p53信号通路抑制增殖并触发HCC细胞凋亡。