Fucoidan Derived from Undaria pinnatifida Induces Apoptosis in Human Hepatocellular Carcinoma SMMC-7721 Cells via the ROS-Mediated Mitochondrial Pathway

Marine Drugs

Lili Yang¹  Peisheng Wang¹  Huaxin Wang¹  Qiaomei Li¹  Hongming Teng¹  Zhichao Liu¹  Wenbo Yang¹  Lin Hou² 

[1] Department of Biotechnology, Dalian Medical University, Dalian 116044, China; E-Mails:;College of Life Science, Liaoning Normal University, Dalian 116081, China

关键词: apoptosis;    fucoidan;    hepatocellular carcinoma;    reactive oxygen species;   

DOI  :  10.3390/md11061961

来源: mdpi

【 摘 要 】

Fucoidans, fucose-enriched sulfated polysaccharides isolated from brown algae and marine invertebrates, have been shown to exert anticancer activity in several types of human cancer, including leukemia and breast cancer and in lung adenocarcinoma cells. In the present study, the anticancer activity of the fucoidan extracted from the brown seaweed Undaria pinnatifida was investigated in human hepatocellular carcinoma SMMC-7721 cells, and the underlying mechanisms of action were investigated. SMMC-7721 cells exposed to fucoidan displayed growth inhibition and several typical features of apoptotic cells, such as chromatin condensation and marginalization, a decrease in the number of mitochondria, and in mitochondrial swelling and vacuolation. Fucoidan-induced cell death was associated with depletion of reduced glutathione (GSH), accumulation of high intracellular levels of reactive oxygen species (ROS), and accompanied by damage to the mitochondrial ultrastructure, depolarization of the mitochondrial membrane potential (MMP, Δψm) and caspase activation. Moreover, fucoidan led to altered expression of factors related to apoptosis, including downregulating Livin and XIAP mRNA, which are members of the inhibitor of apoptotic protein (IAP) family, and increased the Bax-to-Bcl-2 ratio. These findings suggest that fucoidan isolated from U. pinnatifida induced apoptosis in SMMC-7721 cells via the ROS-mediated mitochondrial pathway.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.