Cyanidin 3- <i>O</i> -β- <scp>d</scp> -Glucoside from Black Bean Inhibits the Migration of Vascular Smooth Muscle Cells in the Presence of Adipocytes

Background The potential of cyanidin 3- O -β-D-glucoside (C3G), known for its anti-obesity and anti-diabetic properties, in suppressing arteriosclerosis progression remains unexplored. Objectives This study aimed to elucidate whether C3G prevents or ameliorates arteriosclerosis by investigating the effects of C3G on the transformation, proliferation, and migration of vascular smooth muscle cells (SMCs). Herein, we evaluated the effects of C3G on the migratory ability of SMCs in the presence of adipocytes. Materials and Methods SMCs and 3T3-L1 adipocytes were cocultured in a Boyden chamber, with SMCs positioned in the upper chamber and pre-adipocytes in the lower chamber. Pre-adipocytes were initially seeded in the lower chamber and prompted to undergo differentiation over days 0, 2, 4, 6, and 8. SMCs were seeded in the upper chamber. The quantification of cells that migrated through the membrane was carried out. The migratory potential of SMCs within the SMC/adipocyte coculture (SACC) setup was assessed by placing the upper chamber into wells containing adipocytes, with or without 0.1% C3G. Results The findings indicated that the accumulation of lipid droplets in adipocytes increased as the differentiation stage progressed. The amount of lipid droplets that accumulated upon the addition of C3G was significantly lower than that in the control. C3G was found to inhibit the active form of plasminogen activator inhibitor-1 (PAI-1) while enhancing the levels of the anti-inflammatory adipocytokine adiponectin. In the SACC, SMC migration increased alongside lipid droplet accumulation in adipocytes. We revealed that C3G decreased the active form of PAI-1 in the SACC and suppressed vascular SMC migration. Conclusion C3G inhibited the migration of SMCs in the SACC, highlighting its potential as a compound that can prevent arteriosclerosis and thrombus formation progression by suppressing hyperplasia of the vascular intima.