Background: The cause of atherosclerosis is not known, and therefore the current treatment options are limited. In the present study, we aimed to investigate the effects of Phoenixin 20 and its receptor G protein-coupled receptor 173 (GPR173) against ox-LDL-induced endothelial dysfunction.Materials and Methods: Human aortic endothelial cells (HAECs) were treated with 10 μg/ml ox-LDL in the presence or absence of phoenixin 20. Gene expression of GPR173, ICAM-1, VCAM-1, IL-1β, IL-8, MCP-1, and NOX-4 were measured by real time PCR. Protein expression was assayed by western blot analysis. Secretions of pro-in ammatory cytokines were measured by ELISA. The attachment of THP-1 monocytes to HAECs was detected using calcein-AM staining. Transcriptional activity of NF-κB was measured using dual-luciferase reporter assay.Results: Our ndings indicate that ox-LDL signi cantly lowered the expression of GPR173 in HAECs and triggered an increase in ROS, NOX-4, and proin ammatory cytokine expression. Importantly, we demonstrate that agonism of GPR173 using phoenixin 20 signi cantly ameliorated these harmful effects of ox-LDL. We also show that agonism of GPR173 can prevent the attachment of monocytes to endothelial cells, which is an important therapeutic approach to prevent atherogenesis.
Conclusion:Here, for the rst time to our knowledge, we provide a basis for future research on the role of GPR173 as a new potential treatment against atherosclerosis.