A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine

Abstract Preclinical Research Oxidized low‐density lipoprotein (ox‐ LDL ) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP 21, inhibits the bioactivity of ox‐ LDL via direct binding to ox‐ LDL . Here, we investigated the effect of BP 21 on the mRNA expression of proinflammatory mediators induced by two major components of ox‐ LDL , oxidized‐ and lyso‐phosphatidylcholine (ox‐ PC and LPC ), in monocytes/macrophages ( THP ‐1 cells) and adipocytes (3 T 3‐ L 1 cells). In THP ‐1 cells, BP 21 markedly reduced the mRNA expression of interleukin ( IL )‐6, adipocyte fatty acid‐binding protein ( aP 2), tumor necrosis factor‐α, and mitogen‐activated protein kinase phosphatase‐1, which are induced by one of the major bioactive components of ox‐ PC , 1‐palmitoyl‐2‐(5′‐oxo‐valeroyl)‐ sn ‐glycero‐3‐phosphocholine ( POVPC ), and reduced the mRNA expression of IL ‐6, the ox‐ LDL ‐specific scavenger receptor CD 36, and aP 2 induced by LPC . In adipocytes, the mRNA expression of IL ‐1β as an adipokine and aP 2 is highly induced by ox‐ PC and LPC , and BP 21 markedly reduced the mRNA expression of IL ‐1β and aP 2 induced by POVPC and LPC . Furthermore, BP 21 specifically bound to LPC and POVPC in a dose‐dependent manner. These results suggest that BP 21 may be useful lead for the potential treatment and prevention of inflammatory diseases caused by ox‐ PC and LPC .