School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun, 130117, P. R. China.
Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, P. R. China.
Chem Biodivers. 2021 Jun;18(6):e2100063. doi: 10.1002/cbdv.202100063. Epub 2021 Apr 27.
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.
宝藿苷 I 是从朝鲜淫羊藿中分离得到的一种黄酮类化合物,具有多种药理活性。然而,其在肝癌中的作用尚不清楚。本研究旨在探讨宝藿苷 I 对人肝癌细胞系 QGY7703 的抑制作用及其机制。以 QGY7703 细胞为模型,在体外评估宝藿苷 I 的功能。通过 CCK-8、乳酸脱氢酶释放和侵袭试验证实了宝藿苷 I 对 QGY7703 细胞生长、增殖和侵袭的影响。通过流式细胞术分析细胞凋亡,通过 Western blot 定量测定裂解 Caspase-3、Bax 和 Bcl-2 的水平。Western blot 分析、NF-κB 的核转位和 Q-PCR 用于测量受影响分子的表达。在 QGY7703 细胞中,宝藿苷 I 诱导了与 NF-κB 通路相关的分子表达。在肿瘤模型中也证实了宝藿苷 I 对 QGY7703 细胞的毒性。宝藿苷 I 的浓度为 10 μM 时,对 QGY7703 细胞有明显的毒性作用。该化合物通过诱导细胞凋亡和下调 NF-κB 信号通路,显著抑制 QGY7703 细胞的增殖。因此,宝藿苷 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。