>
Fa   |   Ar   |   En
   Miglitol,an anti-diabetic drug,inhibits oxidative stress-induced apoptosis and mitochondrial ROS over-production in endothelial cells by enhancement of amp-activated protein Kinase  
   
نویسنده aoki c. ,suzuki k. ,yanagi k. ,satoh h. ,niitani m. ,aso y.
منبع journal of pharmacological sciences - 2012 - دوره : 120 - شماره : 2 - صفحه:121 -128
چکیده    Endothelial dysfunction caused by oxidative stress plays a key role in atherogenesis. this study investigated whether the anti-diabetic drug miglitol,an α-glucosidase inhibitor,which is currently available in clinical practice,can prevent endothelial cell apoptosis and whether it might restore impaired vascular relaxation under oxidative stress. the bend.3 cells,a microvascular endothelial cell line,were pre-treated with various concentrations of miglitol and then were incubated with h2o 2 for 1 -2 h. treatment of bend.3 cells with miglitol resulted in the protection of cell viability,suppression of mitochondrial superoxide production,and dna strand breakage under the oxidative stress. these effects of miglitol were associated with the activation of ampactivated protein kinase (ampk) and the phosphorylation of endothelial nitric oxide synthase (enos). in aortic rings with endothelium,acetylcholine (ach)-induced relaxation was attenuated by h2o2. we found that this impaired relaxation was restored by acute treatment with miglitol. compound c,an ampk inhibitor,inhibited the amelioration of vascular relaxations treated with miglitol. these results suggest that miglitol might protect against endothelial cells damage under oxidative stress via inhibition of endothelial cell apoptosis and mitochondrial superoxide production,which are mediated by the activation of ampk and the phosphorylation of enos. © 2012 the japanese pharmacological society.
کلیدواژه AMP-activated protein kinase (AMPK); Endothelial cell; Miglitol; Oxidative stress
آدرس department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan, department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan, department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan, department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan, department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan, department of endocrinology and metabolism,dokkyo medical university,mibu,tochigi 321-0293, Japan
 
     
   
Authors
  
 
 

Copyright 2023
Islamic World Science Citation Center
All Rights Reserved