The human immunodeficiency virus (HIV) is a lentivirus that results in acquired immunodeficiency syndrome (AIDS). HIV treatment involving chemical therapeutic agents has improved the quality of life of HIV/AIDS patients. The present study demonstrates that a hydroxyproline-containing marine collagen peptide (APHCP) derived from Alaska pollack inhibits HIV-1 infection in the MT-4 human T cell-line. APHCP inhibited HIV-1IIIB-induced cell lysis, syncytia formation, reverse transcriptase activity and viral p24 production at non-cytotoxic concentrations; however, APHCP did not inhibit HIV-2ROD infection in MT-4 cells. This suggests that the anti-HIV activity of APHCP is specific to HIV-1. In addition, substitution of hydroxyproline residues in APHCP with prolines impaired its anti-HIV-1 activity, suggesting that the hydroxyl group of hydroxyprolines is required for the anti-HIV-1 activity of APHCP. These results suggested that the marine peptide APHCP may be a novel drug candidate in the development of next-generation therapeutic agents for the treatment of HIV/AIDS.

Dieckol is a polyphenol compound isolated from brown algae that has anti-oxidant, anti-inflammatory, and anti-tumor activity. We examined the anti-angiogenic effects of dieckol in endothelial cells under hypoxic conditions. Treatment with CoCl 2 , a hypoxic mimetic agent, increased proliferation, adhesion, migration, and tube formation in HUVECs, as well as vessel sprouting in rat aortic rings, which correlated well with increased expression of hypoxia-inducible factor 1-alpha (HIF1α) and β1-integrin. Dieckol suppressed CoCl 2 -induced adhesion, migration, and tube formation in HUVECs and vessel sprouting in rat aortic rings. Dieckol treatment decreased CoCl 2 -induced overexpression of HIF1α and its downstream signaling molecules, including β1-integrin/Fak, Akt/eNOS, and p38 MAPK. These results suggest that dieckol is a novel angiogenesis inhibitor and a potential treatment for angiogenesis-dependent diseases in humans, such as malignant tumors.