Abstract
3-hydroxybenzaldehyde (3-HBA) is a precursor compound for phenolic compounds like Protocatechuic aldehyde (PCA). From recent reports, PCA has shown vasculoprotective potency, but the effects of 3-HBA remain unclear. The aim of this study is to investigate the vasculoprotective effects of 3-HBA in endothelial cells, vascular smooth muscle cells and various animal models. We tested effects of 3-HBA in both vitro and vivo. 3-HBA showed that it prevents PDGF-induced vascular smooth muscle cells (VSMCs) migration and proliferation from MTS, BrdU assays and inhibition of AKT phosphorylation. It arrested S and G0/G1 phase of VSMC cell cycle in PI staining and it also showed inhibited expression levels of Rb1 and CD1. In human umbilical vein endothelial cells (HUVECs), 3-HBA inhibited inflammatory markers and signaling molecules (VCAM-1, ICAM-1, p-NF-κB and p-p38). For ex vivo, 3-HBA has shown dramatic effects in suppressing the sprouting from aortic ring of Spargue Dawley (SD) rats. In vivo data supported the vasculoprotective effects of 3-HBA as it inhibited angiogenesis from Matrigel Plug assay in C57BL6 mouse, prevented ADP-induced thrombus generation, increased blood circulation after formation of thrombus, and attenuated neointima formation induced by common carotid artery balloon injury of SD rats. 3-HBA, a novel therapeutic agent, has shown vasculoprotective potency in both in vitro and in vivo.
Highlights
Atherosclerosis is a multi-factor disease process including outgrowth and migration of vascular smooth muscle cells (VSMCs), endothelial dysfunction, chronic inflammation, plaque formation, and rupture and arterial thrombosis
Recent evidence suggests that vascular endothelial inflammatory processes are critical in the initiation of atherosclerosis.[33]
It was necessary to assess the vasoprotective effect of 3-HBA in endothelial cells
Summary
Atherosclerosis is a multi-factor disease process including outgrowth and migration of vascular smooth muscle cells (VSMCs), endothelial dysfunction, chronic inflammation, plaque formation, and rupture and arterial thrombosis. Previous studies on atherosclerosis have shown that the disease is characterized by the increased production of proteins such as VCAM-1, ICAM-1, phosphorylated AKT, CD1, and matrix metalloproteinases (MMPs) and the generation of reactive oxygen species (ROS).[1,2,3,4,5] increased VSMC proliferation and migration, increased expression of adhesion molecules on the surfaces of endothelial cells, augmented platelet aggregation, and inflammatory angiogenesis have been observed.[6,7,8,9]. The latest findings show that these compounds have therapeutic effects for the treatment of various diseases such as cancer and vascular and renal diseases.[11,12,13,14] With regard to atherosclerosis, benzaldehydes are reported as potent inhibitors of lipoprotein-associated phospholipase A2 [15] and are capable upregulators of ABCA1[16]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
