Pinitol protects against ox-LDL-induced endothelial inflammation and monocytes attachment.
2021
ABSTRACT Atherosclerosis is a cardiovascular disease that affects a majority of people around the world at old age. Atherosclerosis is slow to develop and challenging to treat. Endothelial dysfunction caused by oxidative stress, inflammation, and other pathological factors drives the process of atherogenesis. LOX-1 is one of the main scavenging receptors for ox-LDL and contributes to atherogenesis by inducing overproduction of ROS, increased expression of proinflammatory cytokines, and secretion of cellular adhesion molecules. Additionally, activation of LOX-1 inhibits the expression of KLF2, a key protective factor against atherosclerosis. In this study, we investigated the effects of pinitol, and naturally occurring cyclic polyol, on endothelial dysfunction induced by ox-LDL. Our findings show that pinitol revealed a good safety profile, as evidenced by reducing LDH release in human aortic endothelial cells. In our experiments, pinitol reduced the production of ROS and expression of IL-6 and MCP-1 induced by ox-LDL. Pinitol also significantly reduced the attachment of THP-1 monocytes to endothelial cells via downregulation of VCAM-1 and E-selectin. Importantly, we found that pinitol reduced the expression of LOX-1 induced by ox-LDL and rescued the expression of KLF2, which is dependent on ERK5 expression. Together, our findings provide notable evidence that pinitol may have potential implication in the prevention and treatment of atherosclerosis.
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