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Article Abstract
The present study explored the molecular mechanism by which licochalcone B induces the cell cycle arrest and apoptosis in human hepatoma cell HepG2. Initial extraction and identification were performed by HPLC, UPLC-TOF-MS/MS, and NMR analysis, respectively. Licochalcone B inhibited the HepG2 growth with IC (110.15 μM) after 24 h, caused morphological distortion, and seized the cell cycle in the G2/M phase (cell arrest in G2/M:43.1 ± 2.2% for 120 μM versus 23.7 ± 1.2% for control), as well as induced apoptosis and intracellular ROS generation. Furthermore, exposure to licochalcone B markedly affected the cell cycle (up/down regulation) at mRNA and protein levels. Apoptosis was induced through the activation of receptor-mediated and mitochondrial pathways. The inhibition of Caspase 8 and Caspase 9 proteins abolished the licochalcone B induced apoptosis. The present work suggested that licochalcone B may further be identified as a potent functional food component with specific health benefits.
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