保火苷Ⅰ通过凋亡信号和NF-kB通路抑制肝癌细胞增殖,Chemistry & Biodiversity

当前位置： X-MOL 学术 › Chem. Biodivers. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

保火苷Ⅰ通过凋亡信号和NF-kB通路抑制肝癌细胞增殖
Chemistry & Biodiversity ( IF 2.3 ) Pub Date : 2021-04-27 , DOI: 10.1002/cbdv.202100063
Yunlong Sun ₁ , Bo Pang ₂ , Yingzhe Wang ₁ , Jinglei Xiao ₁ , Dacheng Jiang ₁

Affiliation

保火苷Ⅰ是从淫羊藿中分离得到的黄酮类化合物，具有多种药理活性。然而，其在肝癌中的作用仍不清楚。本研究旨在探讨保活苷 I 对人肝细胞癌 (HCC) 细胞系 QGY7703 的抑制作用及其机制。以QGY7703细胞为模型评价保活苷Ⅰ的体外功能. 保活苷Ⅰ对QGY7703细胞生长、增殖和侵袭性的影响通过CCK-8、乳酸脱氢酶释放和侵袭试验证实。通过流式细胞术分析细胞凋亡，并通过蛋白质印迹定量切割的 Caspase-3、Bax 和 Bcl-2 的水平。蛋白质印迹分析、NF-κB 的核易位和 Q-PCR 用于测量受影响分子的表达。在QGY7703细胞中，保火苷Ⅰ诱导NF-κB通路相关分子的表达。保活苷Ⅰ对QGY7703细胞的毒性也在体内得到证实, 在肿瘤模型中。保活苷Ⅰ从10 μM的浓度开始对QGY7703细胞有显着的毒性作用。该化合物通过诱导细胞凋亡和下调 NF-κB 信号通路显着抑制 QGY7703 细胞的增殖。因此，保活苷I是一种新型候选药物，为HCC治疗的临床策略开辟了新的可能性。

"点击查看英文标题和摘要"

Baohuoside I Inhibits the Proliferation of Hepatocellular Carcinoma Cells via Apoptosis Signaling and NF-kB Pathway

Baohuoside I is a flavonoid isolated from Epimedium koreanum Nakai and has many pharmacological activities. However, its role in liver cancer remains unclear. This study aimed to investigate the inhibitory effect of Baohuoside I on the Human Hepatocellular Carcinoma (HCC) cell lines QGY7703, and underlying mechanisms. QGY7703 cells were used as the model to assess the function of Baohuoside I in vitro. The effects of Baohuoside I on QGY7703 cells’ growth, proliferation, and invasiveness were confirmed by CCK-8, lactate dehydrogenase release, and invasion assays. Cell apoptosis was analyzed by flow cytometry, and the levels of cleaved Caspase-3, Bax, and Bcl-2 were quantified by western blot. Western blot analysis, nuclear translocation of NF-κB, and Q-PCR were used to measure the expression of affected molecules. In QGY7703 cells, Baohuoside I induced the expression of molecules related to NF-κB pathway. The toxicity of Baohuoside I on QGY7703 cells was also confirmed in vivo, in a tumor model. Baohuoside I had a significant toxic effect on QGY7703 cells from a concentration of 10 μM. This compound significantly inhibited the proliferation of QGY7703 cells by inducing apoptosis and downregulating NF-κB signaling pathway. Thus, Baohuoside I is a novel candidate drug and opens new possibilities of clinical strategies for HCC treatment.

更新日期：2021-06-15

点击分享查看原文

点击收藏

阅读更多本刊新发论文本刊介绍/投稿指南