Ursolic acid causes DNA-damage, P53-mediated, mitochondria- and caspase-dependent human endothelial cell apoptosis, and accelerates atherosclerotic plaque formation in vivo

Vitamin E as a Functional and Biocompatibility Modifier of Synthetic Hemodialyzer Membranes: An Overview of the Literature on Vitamin E-Modified Hemodialyzer Membranes

“…Endothelial cells are highly prone to oxidative stress that can be prevented both in vitro and in vivo by antioxidants and mitochondrial protection agents [18,19,20]. ROS and receptor-dependent effects of cytokines and modified low-density lipoprotein (LDLs) are associated with an impaired energy function and apoptotic signaling of mitochondria, and cause ER stress through either Ca-dependent or -independent signaling in different types of cells [21,22].…”

Enhancement of Platelet Aggregation by Ursolic Acid and Oleanolic Acid

“…However, recent studies involving the circulatory system have been more equivocal. UA reportedly accelerates atherosclerotic plaque formation in vivo (Messner et al , 2011), contrary to another study showing the protective effect of UA against diabetes-accelerated atherosclerosis (Ullevig et al , 2011). OA directly elicits aggregation of isolated platelets (Liu et al , 2013), a process that is critically involved in the initiation of cardiovascular events (Liu et al , 2013), although other studies addressed the antiplatelet effect of UA and OA and anticoagulant activity of OA (Jin et al , 2004a; Jin et al , 2004b; Babalola et al , 2013).…”

Effects of Vasoactive Chinese Herbs on the Endothelial NO System

“…In the rat carotid artery injury model, ursolic acid has been demonstrated to inhibit neointima formation [51]. In contrast, a recent study has shown that oral treatment of apolipoprotein E-knockout mice with ursolic acid for 24 weeks accelerates atherosclerotic plaque formation in a dose-dependent manner [52]. In the latter study, ursolic acid inhibited endothelial proliferation and induced endothelial cell death.…”

“…In the latter study, ursolic acid inhibited endothelial proliferation and induced endothelial cell death. Ursolic acid caused DNA damage, followed by the activation of a p53-, BAK-, and caspase-dependent cell-death pathway [52]. Further studies are needed to clarify this controversy.…”