Galangin reduces vascular endothelial cell dysfunction via Heme oxygenase-1 signaling.

Abstract

As one of the independent risk factors for atherosclerosis (AS), oxidized low-density lipoprotein (ox-LDL) can trigger damage to the vascular intima and induce the expression of various adhesion molecules. This study aimed to explore the effects of galangin, an extract of galangal, on ox-LDL-induced vascular endothelial cells. The effects of different concentrations of galangin or ox-LDL on the metabolic activity of vascular endothelial cells were determined using the CCK8 assay. Afterward, the role of galangin in the expression levels of inflammatory factors was assessed using RT-qPCR and Western blotting. In addition, the influences of galangin on apoptosis and endothelial-mesenchymal transition (EndMT) were also evaluated. Through molecular docking, the Heme oxygenase-1 (HO-1) signaling pathway was proposed, and then the effects of the HO-1 signaling pathway on the regulatory roles of galangin were evaluated. In this study, galangin was found to effectively increase the metabolic activity of ox-LDL-induced cells in a concentration-dependent manner. In addition, galangin was found to reduce ox-LDL-induced cell inflammation, apoptosis, and EndMT. Moreover, galangin could combine with HO-1 and regulate the HO-1 signaling pathway. The effects of galangin on cells were shown to be through the HO-1 signaling pathway. To sum up, galangin reduced ox-LDL-induced inflammation, apoptosis, and EndMT of vascular endothelial cells via regulating the HO-1 signaling pathway.