Bergamot regulates oxidized low density lipoprotein induced inflammation and foam cell formation of human umbilical vein endothelial cells by regulating SIRT1/NF κB pathway

Abstract

Purpose: To investigate the effects of bergamot (BGM) on the progression of atherosclerosis, and to unravel the mechanism of action. Methods: Oxidized low-density lipoprotein (Ox-LDL)-induced HUVECs were used as an in vitro model of atherosclerosis. CCK-8, flow cytometry (FCM), and enzyme-linked Immunosorbent assay (ELISA) assays were performed to confirm the effects of BGM on the viability and inflammation of ox-LDL-induced HUVECs. Oil-red staining and immunoblot tests were conducted to determine the effects of BGM on foam cell formation and macrophage polarization. Furthermore, The mechanism of action of BGM was examined by immunoblot studies. Results: BGM alleviated the ox-LDL-stimulated decline in HUVEC cell viability, and the ox-LDL-stimulated HUVEC inflammation, but inhibited ox-LDL-stimulated foam cell formation and macrophage polarization in vitro (p < 0.05). In addition, BGM regulated SIRT1/NF-κB pathway, thereby alleviating atherosclerosis (p < 0.05). Conclusion: BGM regulates OX-LDL-induced inflammation and foam cell formation of HUVECs by mediating SIRT1/NF-κB pathway, and therefore can potentially serve as a drug for the treatment of atherosclerosis.