Bergenin ameliorates the progression of atherosclerosis by inhibiting oxidative stress, inflammation, and monocytes adhesion in human umbilical vein endothelial cells

BackgroundBergenin is a type of polyphenol derived from various medicinal plants and has multiple biological functions, including antioxidant, anti-cancerous, and anti-inflammatory activity. However, the role of bergenin in atherosclerosis (AS) development has not been detected yet. Here, human umbilical vein endothelial cells (HUVECs) were used to investigate the effects of bergenin on TNF-alpha-induced oxidative stress, inflammation, and monocyte adhesion in vitro. MethodsCell viability of HUVECs was assessed by cell counting kit-8 (CCK-8) assay. Western blotting was performed to evaluate the levels of apoptosis- or signaling-related proteins. Intracellular oxidative stress levels were detected by evaluating reactive oxygen species (ROS) production, malondialdehyde (MDA) level, and superoxide dismutase (SOD) activity in HUVECs. The effects of bergenin on monocyte adhesion to HUVECs were detected by measuring the protein and expression levels of adhesion molecules. ResultsBergenin promoted the viability and inhibited the apoptosis in TNF-alpha-treated HUVECs. The increased oxidative stress induced by TNF-alpha was significantly suppressed by bergenin in a concentration-dependent manner. Bergenin reduced the protein and expression levels of adhesion molecules in TNF-alpha-treated HUVECs. Human leukemic monocyte (U973) adhesion to HUVECs was promoted by TNF-alpha treatment and significantly inhibited by bergenin. In addition, bergenin blocked the activation of NF-kappa B signaling in TNF-alpha-treated HUVECs. ConclusionBergenin inhibited TNF-alpha-induced apoptosis and oxidative stress in HUVECs and suppressed monocyte adhesion to HUVECs by inactivating NF-kappa B signaling pathway.