Abstract
We have previously shown that sulforaphane not only inhibits formation of advanced glycation end products (AGEs) but also exerts anti-inflammatory effects on AGE-exposed human umbilical vein endothelial cells (HUVECs) and AGE-injected rat aortae. Here we examined the effects of aqueous extract of glucoraphanin-rich broccoli sprouts on formation of AGEs and then investigated whether the extract could attenuate inflammatory or oxidative stress reactions in tumor necrosis factor-alpha (TNF-α)- or AGE-exposed HUVECs. Fresh broccoli sprouts were homogenized in phosphate-buffered saline and filtered through a gauze. After centrifugation, clear extract was obtained. AGE formation was measured by enzyme-linked immunosorbent assay. Gene expression was evaluated by real-time reverse transcription-polymerase chain reaction. Reactive oxygen species (ROS) generation were measured using a fluorescent dye. Five percent broccoli sprout extract inhibited the formation of AGEs, reduced basal gene expressions of monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1,) and receptor for AGEs (RAGE), and upregulated endothelial nitric oxide synthase (eNOS) mRNA levels in HUVECs. TNF-α upregulated MCP-1, ICAM-1, and RAGE mRNA levels in HUVECs, all of which were attenuated by the treatment with 1% broccoli sprout extract. Pretreatment of 1% broccoli sprout extract prevented the ROS generation in HUVECs evoked by AGEs. The present study demonstrates that sulforaphane-rich broccoli sprout extract could inhibit the AGE-RAGE axis and exhibit anti-inflammatory actions in HUVECs. Supplementation of sulforaphane-rich broccoli sprout extract may play a protective role against vascular injury.
Highlights
Sugars, such as glucose, glyceraldehyde, and methylglyoxal, can react nonenzymatically with the amino groups of lipids, proteins, and nucleic acids to form senescent macromolecules termed “advanced glycation end products (AGEs),” whose process has been shown to progress under inflammatory and hyperglycemic conditions [1,2,3,4,5,6,7,8,9]
In this study, we examined the effects of aqueous extract of a precursor of sulforaphane, glucoraphanin-rich broccoli sprouts on AGE formation in vitro and investigated whether the extract could attenuate the inflammatory reactions in tumor necrosis factor-α (TNF-α)- or AGE-exposed human umbilical vein endothelial cells (HUVECs)
We investigated the effects of 1% broccoli sprout extract on monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecule-1 (ICAM-1), and endothelial nitric oxide synthase (eNOS) gene expressions in TNF-α-exposed HUVECs
Summary
Sugars, such as glucose, glyceraldehyde, and methylglyoxal, can react nonenzymatically with the amino groups of lipids, proteins, and nucleic acids to form senescent macromolecules termed “advanced glycation end products (AGEs),” whose process has been shown to progress under inflammatory and hyperglycemic conditions [1,2,3,4,5,6,7,8,9]. Accumulating evidence has suggested that AGEs alter the structural integrity and function of macromolecules and evoke oxidative stress generation and inflammatory reactions in various types of cells and organs through the interaction with a receptor for AGEs (RAGE), contributing to the development and progression of numerous aging- and diabetes-related complications, including atherosclerotic cardiovascular disease, cancer growth and metastasis, osteoporosis, and Alzheimer’s disease [1,2,3,4,5,6,7,8,9]. In this study, we examined the effects of aqueous extract of a precursor of sulforaphane, glucoraphanin-rich broccoli sprouts on AGE formation in vitro and investigated whether the extract could attenuate the inflammatory reactions in tumor necrosis factor-α (TNF-α)- or AGE-exposed human umbilical vein endothelial cells (HUVECs)
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