Icariin improves eNOS/NO pathway to prohibit the atherogenesis of apolipoprotein E-null mice

Abstract

These findings suggested icariin could improve eNOS / NO-pathway to prohibit the atherogenesis of apolipoprotein E null mice by restraining oxidative stress.

Icariin, an Anti-atherosclerotic Drug from Chinese Medicinal Herb Horny Goat Weed

“…Previous studies have suggested that Icariin attenuated the development of atherosclerosis in several animal models, including ApoE -/- mice ( Xiao et al, 2015 , 2017 ; Wang et al, 2016 ), rats ( Hu et al, 2015b ), and rabbits ( Zhang et al, 2013 ). The atheroprotective mechanisms of Icariin are exerted through anti-oxidative, anti-inflammatory, anti-thrombotic, and lipid-modulatory effects.…”

“…In terms of the important role of SIRT6 in regulating endothelial dysfunction and atherosclerosis ( Liu et al, 2016 ; Xu et al, 2016a , c ; Zhang et al, 2016 ), Icariin has recently been reported as a SIRT6 pharmacological activator in vitro and in vivo ( Chen et al, 2015 ), pinpointing the potential contribution of SIRT6 activation to the atheroprotective effects of Icarrin. The endothelial protective effects of Icariin contributed to upregulation of eNOS-dependent NO production in ApoE -/- mice fed a high fat diet ( Xiao et al, 2017 ).…”

Golgi apparatus fragmentation participates in oxidized low‐density lipoprotein‐induced endothelial cell injury

“…Ox‐LDL, as an important trigger of AS, has been reported to induce endothelial dysfunction via reducing eNOS activity and NO level . A previous study demonstrated that icariin could prohibit atherogenesis by increasing NO concentration and eNOS expression . In this study, we further investigated the role of GA fragmentation in ox‐LDL‐induced endothelial dysfunction.…”

“…24,26 A previous study demonstrated that icariin could prohibit atherogenesis by increasing NO concentration and eNOS expression. 27 In this study, we further investigated the role of GA fragmentation in ox-LDL-induced endothelial dysfunction. To mitigate GA fragmentation, HUVECs were transfected with GRASP65 plasmid.…”

Endothelial Nitric Oxide Synthase Gene Polymorphism and Coronary Artery Disease in Asian Populations

“…Therefore, a reduction in the bioavailability of vascular NO will precipitate atherosclerosis process. Functional studies were used to validate these protective effects by using gene disrupted mice that confirmed the role of NO in limiting the vascular atherosclerotic damage 14,47,48 . However, the causal relation between eNOS gene polymorphisms and CAD can't be simply confirmed in human because the aetiology for CAD is stratified by other risk factors such as obesity, smoking, hypertension, diabetes and lifestyle 49,50 .…”