首页|黄酮类化合物GL-V9对肝细胞癌细胞的抑制作用及其机制

黄酮类化合物GL-V9对肝细胞癌细胞的抑制作用及其机制

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目的 全球范围内,肝细胞癌是最常见的恶性肿瘤之一,尤其在中国,其发病率极高。由于当前的治疗手段疗效有限,肝细胞癌患者的预后通常不佳。本研究旨在探讨黄酮类化合物GL-V9对肝细胞癌细胞的抑制效果及其作用机制。方法 采用Cell counting kit-8(CCK-8法)检测不同浓度的GL-V9在不同时间对肝细胞癌细胞系Bel-7404的细胞增殖影响。通过平板克隆实验测定GL-V9对Bel-7404细胞增殖能力的影响。通过流式细胞术分析GL-V9对Bel-7404细胞凋亡率的影响。采用蛋白免疫印迹法检测GL-V9对Bel-7404细胞中自噬标志物LC3和Beclin-1的表达变化。结果 GL-V9显著地抑制了肝细胞癌细胞系Bel-7404的增殖,导致肝细胞癌细胞的细胞凋亡率增加,以及LC3和Beclin-1的表达显著变化。结论 GL-V9对肝细胞癌细胞的显著抑制效应可能与GL-V9作用下肝细胞癌细胞系中自噬通路的激活有关。
Inhibitory effect and mechanism of hepatocellular carcinoma cells upon treatment with the flavonoid compound GL-V9
Objective Hepatocellular carcinoma is one of the most common malignant tumors in the world,especially in China.The prognosis for patients with hepatocellular carcinoma is often poor due to the limited effectiveness of current treatments.The aim of this study was to investigate the inhibitory effect and mechanism of flavonoid GL-V9 on hepatocellu-lar carcinoma cells.Methods Cell counting kit-8(CCK-8 method)was used to detect the effects of different concentrations of GL-V9 on cell proliferation of hepatocellular cancer cell line Bel-7404 at different times.The effect of GL-V9 on the proliferation of Bel-7404 cells was determined by plate cloning.The effect of GL-V9 on apoptosis rate of Bel-7404 cells was analyzed by flow cytometry.The expression of autophagy markers LC3 and Beclin-1 in Bel-7404 cells were detected by Western blot assay with GL-V9.Results GL-V9 significantly inhibited the proliferation of hepatocellular carcinoma cell line Bel-7404,resulting in increased apoptosis rate of hepatocellular carcinoma cells,and significant changes in LC3 and Beclin-1 expression.Conclusion The significant inhibitory effect of GL-V9 on hepatocellular carcinoma cells may be relat-ed to the activation of autophagy pathway in hepatocellular carcinoma cell lines under the action of GL-V9.

GL-V9Hepatocellular carcinomaApoptosisAutophagy

黄亚妹

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东南大学医学院病理学与病理生理学系,江苏南京 210009

GL-V9 肝细胞癌 凋亡 自噬

2024

中国当代医药
中国保健协会 当代创新(北京)医药科学研究院

中国当代医药

影响因子:1.215
ISSN:1674-4721
年,卷(期):2024.31(4)
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