Anti-hepatocellular Carcinoma Activity and Related Mechanism of Apigenin-7-O-Glucoside

Abstract

Objective To investigate the inhibitory effect of apigenin-7-o-glucoside (AGL) on the viability of Huh7 cells and tumor growth in Huh7-xenograft tumor nude mice. Methods CCK-8 was used to detect the proliferation inhibitory effect and the half inhibitory concentration of AGL on Huh7 cells. The mitochondrial membrane potential measurement was used to analyze the early apoptosis of Huh7 cells after AGL treatment. Flow cytometry was used to analyze the effect of AGL on Huh7 cell apoptosis, and Western blot was used to explore the expression level of the proteins associated with apoptosis and inflammation, as well as the possible related mechanism. In Huh7-xenograft tumor nude mice, vernier caliper was used to measure tumor volume to analyze the effect of AGL on tumor growth rate. HE staining was used to observe the pathological state of mouse organs, and the inflammation-related factors in serum were detected with ELISA. Results After Huh7 cells were treated with AGL, the mitochondrial membrane potential reduced, the content of ROS increased and the apoptosis rate was increased to 25.23% by 50 μmol/L AGL treatment; while the expression levels of Bax, Bad, Cleaved Caspase-3 and Cleaved Caspase-9 increased, and the expression levels of Bcl2 and Bcl-xL decreased, the phosphorylation level of NF-κB, IKKα/β and IκBα decreased; the tumor growth rate decreased, the serum IL-6 and TNF-α levels significantly decreased, while the IL-2 and IL-10 levels increased. Conclusion AGL could promote the apoptosis of Huh7 cells and relieve the tumor development in Huh7-xenograft tumor nude mice, which may be related to the NF-κB pathway.

Keywords

• apigenin-7-o-glucoside
• huh7 cells
• hepatocellular carcinoma
• nf-κb