کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9157563 1172459 2005 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway
چکیده انگلیسی
Diabetes mellitus is one of the major risk factors for coronary artery disease (CAD). A recent study reported that glimepiride, a new third-generation sulfonylurea, inhibited the formation of atheromatous plaques in high-cholesterol fed rabbits. However, the mechanism by which glimepiride induces atheroprotection remains unknown. In the present study, we tested the hypothesis that glimepiride may stimulate NO production in vascular endothelial cells. Human coronary artery endothelial cells (HCAECs) were treated with glimepiride, glibenclamide or vehicle, and NO release was measured. Akt phosphorylation was evaluated by Western blot. The effects of LY294002, a specific PI3-kinase inhibitor, and antisense oligonucleotides directed to Akt, on glimepiride-induced NO production were examined. Glimepiride (0.1-10 μM), but not glibenclamide, induced NO production, significantly increasing it by 1.8-fold (n = 6, p < 0.05). LY294002 inhibited glimepiride-induced NO production by 68%. Akt was rapidly phosphorylated by glimepiride and antisense oligonucleotides directed to Akt completely inhibited glimepiride-induced NO production. These data demonstrate that glimepiride induces NO production in HCAECs by activating PI3-kinase and Akt, and also suggest that use of glimepiride in type 2 diabetes may show promise for preventing CAD in addition to lowering glucose levels.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Atherosclerosis - Volume 183, Issue 1, November 2005, Pages 35-39
نویسندگان
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