甘草查尔酮 B 从甘草中提取诱导人肝癌细胞 HepG2 凋亡。

Licochalcone B Extracted from Glycyrrhiza uralensis Fisch Induces Apoptotic Effects in Human Hepatoma Cell HepG2.

机构信息

School of Food and Biological Engineering , Hefei University of Technology , Hefei 230009 , People's Republic of China.

College of Biological Engineering , Henan University of Technology , Zhengzhou 450001 , People's Republic of China.

出版信息

J Agric Food Chem. 2019 Mar 27;67(12):3341-3353. doi: 10.1021/acs.jafc.9b00324. Epub 2019 Mar 12.

DOI:10.1021/acs.jafc.9b00324

PMID:30835110

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.

摘要

本研究探讨了甘草查尔酮 B 诱导人肝癌细胞 HepG2 细胞周期停滞和凋亡的分子机制。分别通过 HPLC、UPLC-TOF-MS/MS 和 NMR 分析进行初步提取和鉴定。甘草查尔酮 B 在 24 小时后抑制 HepG2 生长，IC（110.15 μM），引起形态变形，并将细胞周期阻滞在 G2/M 期（细胞阻滞在 G2/M：120 μM 时为 43.1±2.2%，而对照组为 23.7±1.2%），并诱导细胞凋亡和细胞内 ROS 生成。此外，甘草查尔酮 B 的暴露在 mRNA 和蛋白质水平上明显影响细胞周期（上调/下调）。通过受体介导和线粒体途径的激活诱导细胞凋亡。抑制 Caspase 8 和 Caspase 9 蛋白可消除甘草查尔酮 B 诱导的细胞凋亡。本研究表明，甘草查尔酮 B 可能进一步被鉴定为具有特定健康益处的功能性食品成分。