Aqueous Extract of Glucoraphanin‐Rich Broccoli Sprouts Inhibits Formation of Advanced Glycation End Products and Attenuates Inflammatory Reactions in Endothelial Cells

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.

Sulforaphane-Enriched Broccoli Sprouts Pretreated by Pulsed Electric Fields Reduces Neuroinflammation and Ameliorates Scopolamine-Induced Amnesia in Mouse Brain through Its Antioxidant Ability via Nrf2-HO-1 Activation

“…Inhibition of iNOS or NO production, therefore, could mitigate oxidative stress and further inflammatory cascades in neurodegenerative diseases. Previous studies reported that broccoli sprout inhibited inflammation in endothelial cells [39] and in LPS-treated mice [13]. Additionally, sulforaphane inhibited iNOS-mediated NO production in activated microglia [40].…”

Bioactive Compounds and Bioactivities of Brassica oleracea L. var. Italica Sprouts and Microgreens: An Updated Overview from a Nutraceutical Perspective

“…The anti-inflammatory mechanisms of broccoli sprouts are probably associated with the nuclear factor-kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways [27]. Both in vitro and in vivo experiments, as well as clinical trials, mainly exhibit anti-inflammatory effects of broccoli sprouts, which showed high concentrations of sulforaphane and a group of phenolic compounds, including anthocyanins, isoquercetin, chlorogenic and cinnamic acids, via inhibiting inflammatory mediators such as a nitric oxide (NO), decreasing the levels of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and IL-1β, and increasing the levels of anti-inflammatory cytokines such as IL-10 and IL-22 [27,28,55,72,113,114]. For example, a study showed that sulforaphane-enriched broccoli sprouts inhibited activation of the NF-κB signaling pathway and the secretions of inflammatory proteins (inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2), TNF-α, IL-6, IL-1β, and prostaglandin E2 (PGE2)) in microglial cells (BV2) and male ICR (Institute of Cancer Research) mice.…”

Sulforaphane Inhibits MGO-AGE-Mediated Neuroinflammation by Suppressing NF-κB, MAPK, and AGE–RAGE Signaling Pathways in Microglial Cells

“…It is known to have antioxidant, anti-inflammatory, anti-apoptotic, cytoprotective, and anti-diabetic effects [ 17 , 18 ]. The aqueous extract of glucoraphanin-rich broccoli sprouts inhibits AGE formation and AGE-induced inflammatory reactions in endothelial cells and rat aorta [ 19 , 20 ]. Furthermore, SFN-mediated inhibition of AGE–RAGE interaction is known to be responsible for pericyte protection against AGE-induced toxicity [ 21 ].…”