کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5996374 1180662 2016 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation in endothelial cells and rat aorta
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation in endothelial cells and rat aorta
چکیده انگلیسی


- Sulforaphane inhibited the AGEs-induced ROS generation in ECs.
- Sulforaphane inhibited the AGEs-induced RAGE mRNA up-regulation in ECs.
- Sulforaphane suppressed the inflammatory reactions in AGEs-exposed ECs.
- Sulforaphane inhibited the inflammation in aorta of AGEs-injected rats.

Background and AimsAdvanced glycation end products (AGEs)-receptor RAGE interaction evokes oxidative stress and inflammatory reactions, thereby being involved in endothelial cell (EC) damage in diabetes. Sulforaphane is generated from glucoraphanin, a naturally occurring isothiocyanate found in widely consumed cruciferous vegetables, by myrosinase. Sulforaphane has been reported to protect against oxidative stress-mediated cell and tissue injury. However, effects of sulforaphane on AGEs-induced vascular damage remain unclear.Methods and ResultsIn this study, we investigated whether and how sulforaphane could inhibit inflammation in AGEs-exposed human umbilical vein ECs (HUVECs) and AGEs-injected rat aorta. Sulforaphane treatment for 4 or 24 h dose-dependently inhibited the AGEs-induced increase in RAGE, monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecular-1 (VCAM-1) gene expression in HUVECs. AGEs significantly stimulated MCP-1 production by, and THP-1 cell adhesion to, HUVECs, both of which were prevented by 1.6 μM sulforaphane. Sulforaphane significantly suppressed oxidative stress generation and NADPH oxidase activation evoked by AGEs in HUVECs. Furthermore, aortic RAGE, ICAM-1 and VCAM-1 expression in AGEs-injected rats were increased, which were suppressed by simultaneous infusion of sulforaphane.ConclusionThe present study demonstrated for the first time that sulforaphane could inhibit inflammation in AGEs-exposed HUVECs and AGEs-infused rat aorta partly by suppressing RAGE expression through its anti-oxidative properties. Inhibition of the AGEs-RAGE axis by sulforaphane might be a novel therapeutic target for vascular injury in diabetes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nutrition, Metabolism and Cardiovascular Diseases - Volume 26, Issue 9, September 2016, Pages 797-807
نویسندگان
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