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Published on: September 19, 2016
Sulforaphane reduces advanced glycation end products (AGEs)-induced inflammation in endothelial cells and rat aorta
T Matsui1, N Nakamura1, A Ojima1
1Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan.
Background And Aims:
Advanced 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 Results:
In 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.
Conclusion:
The 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.
Insights
Sulforaphane, a compound from cruciferous vegetables, reduces inflammation and oxidative stress in blood vessels damaged by advanced glycation end products (AGEs). This suggests sulforaphane may be a new treatment for diabetic vascular injury.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Advanced glycation end products (AGEs) trigger oxidative stress and inflammation, leading to endothelial cell (EC) damage in diabetes.
- Sulforaphane, derived from cruciferous vegetables, shows protective effects against oxidative stress-induced injury.
- The impact of sulforaphane on AGEs-induced vascular damage is not well understood.
Purpose of the Study:
- To investigate sulforaphane's ability to inhibit inflammation in AGEs-exposed human umbilical vein ECs (HUVECs) and AGEs-injected rat aorta.
- To elucidate the mechanisms by which sulforaphane affects AGEs-induced vascular damage.
Main Methods:
- Dose-dependent sulforaphane treatment of AGEs-exposed HUVECs and AGEs-injected rats.
- Measurement of gene expression for RAGE, MCP-1, ICAM-1, and VCAM-1.
- Assessment of THP-1 cell adhesion to HUVECs.
- Evaluation of oxidative stress generation and NADPH oxidase activation.
- Analysis of aortic RAGE, ICAM-1, and VCAM-1 expression.
Main Results:
- Sulforaphane dose-dependently inhibited AGEs-induced increases in RAGE, MCP-1, ICAM-1, and VCAM-1 gene expression in HUVECs.
- Sulforaphane prevented AGEs-stimulated MCP-1 production and THP-1 cell adhesion to HUVECs.
- Sulforaphane suppressed AGEs-induced oxidative stress and NADPH oxidase activation in HUVECs.
- Sulforaphane reduced elevated aortic RAGE, ICAM-1, and VCAM-1 expression in AGEs-injected rats.
Conclusions:
- Sulforaphane inhibits inflammation in AGEs-exposed HUVECs and rat aorta, partly by suppressing RAGE expression via its antioxidant properties.
- Inhibition of the AGEs-RAGE axis by sulforaphane presents a potential therapeutic strategy for diabetic vascular injury.
