Limits...
The influence of sulforaphane on vascular health and its relevance to nutritional approaches to prevent cardiovascular disease.

Evans PC - EPMA J (2011)

Bottom Line: Oxidation of low-density lipoproteins (LDL) promotes atherosclerosis by enhancing vascular inflammation and foam cell formation.This review focuses on sulforaphane, an isothiocyanate derived from green vegetables, which induces multiple anti-oxidant enzymes via activation of a transcription factor called Nrf2.A deeper understanding of vascular responses to sulforaphane may inform nutritional approaches to prevent vascular inflammation and atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: British Heart Foundation, Cardiovascular Sciences Unit, National Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London, W12 ONN UK.

ABSTRACT
Oxidation of low-density lipoproteins (LDL) promotes atherosclerosis by enhancing vascular inflammation and foam cell formation. The corollary is that diets that stimulate endogenous anti-oxidants may protect against atherosclerosis. This review focuses on sulforaphane, an isothiocyanate derived from green vegetables, which induces multiple anti-oxidant enzymes via activation of a transcription factor called Nrf2. Although studies of cultured cells and experimental animals revealed that sulforaphane can suppress inflammatory activation of vascular cells, the potential beneficial effects of sulforaphane in atherosclerosis have not been studied directly. A deeper understanding of vascular responses to sulforaphane may inform nutritional approaches to prevent vascular inflammation and atherosclerosis.

No MeSH data available.


Related in: MedlinePlus

Model—Consumption of Brassica vegetables may prevent vascular inflammation at atherosusceptible sites. Regions of arteries with relatively uniform geometry are protected from inflammation and atherosclerosis by high shear stress which activates Nrf2. By contrast, branches and bends that are exposed to low, oscillatory shear stress are susceptible to lesion formation. However, dietary consumption of Brassica vegetables may prevent branches and bends from inflammation by activating Nrf2 in endothelial cells
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3405367&req=5

Fig2: Model—Consumption of Brassica vegetables may prevent vascular inflammation at atherosusceptible sites. Regions of arteries with relatively uniform geometry are protected from inflammation and atherosclerosis by high shear stress which activates Nrf2. By contrast, branches and bends that are exposed to low, oscillatory shear stress are susceptible to lesion formation. However, dietary consumption of Brassica vegetables may prevent branches and bends from inflammation by activating Nrf2 in endothelial cells

Mentions: We recently studied the effects of shear stress and sulforaphane on endothelial activation in aortae of mice challenged with lipopolysaccharide (LPS) [70]. Vascular inflammation and atherosclerosis develop predominantly at branches and bends of arteries which are exposed to non-uniform blood flow which exerts relatively low shear stress on vascular endothelium, whereas regions of arteries that are exposed to high shear stress are protected [76, 77]. Pro-inflammatory activation of EC is reduced at high shear sites compared to low shear regions, thus providing a potential explanation for the distinct spatial localisation of lesions [70, 78, 79]. Our findings revealed that high shear stress at atheroprotected sites reduced key measures of EC inflammatory activation, p38 MAP kinase activation and VCAM-1 expression, by activating Nrf2 [70] (Fig. 2). By contrast, EC at a low shear, atherosusceptible site contained inactive (cytoplasmic) Nrf2 and were prone to pro-inflammatory activation. We therefore examined whether pharmacological activation of Nrf2 using sulforaphane would suppress inflammation at susceptible sites. In cultured EC, sulforaphane suppressed p38 activation, VCAM-1 expression and ROS production via Nrf2 [70, 71]. Similarly, sulforaphane suppressed p38 activation and VCAM-1 expression at atherosusceptible sites in wild-type but not in Nrf2-/- mice, indicating that the anti-inflammatory effects of sulforaphane were Nrf2-dependent [70] (Fig. 2). Thus our observations reveal that inflammation at atherosusceptible regions can be prevented by sulforaphane-mediated activation of Nrf2.Fig. 2


The influence of sulforaphane on vascular health and its relevance to nutritional approaches to prevent cardiovascular disease.

Evans PC - EPMA J (2011)

Model—Consumption of Brassica vegetables may prevent vascular inflammation at atherosusceptible sites. Regions of arteries with relatively uniform geometry are protected from inflammation and atherosclerosis by high shear stress which activates Nrf2. By contrast, branches and bends that are exposed to low, oscillatory shear stress are susceptible to lesion formation. However, dietary consumption of Brassica vegetables may prevent branches and bends from inflammation by activating Nrf2 in endothelial cells
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3405367&req=5

Fig2: Model—Consumption of Brassica vegetables may prevent vascular inflammation at atherosusceptible sites. Regions of arteries with relatively uniform geometry are protected from inflammation and atherosclerosis by high shear stress which activates Nrf2. By contrast, branches and bends that are exposed to low, oscillatory shear stress are susceptible to lesion formation. However, dietary consumption of Brassica vegetables may prevent branches and bends from inflammation by activating Nrf2 in endothelial cells
Mentions: We recently studied the effects of shear stress and sulforaphane on endothelial activation in aortae of mice challenged with lipopolysaccharide (LPS) [70]. Vascular inflammation and atherosclerosis develop predominantly at branches and bends of arteries which are exposed to non-uniform blood flow which exerts relatively low shear stress on vascular endothelium, whereas regions of arteries that are exposed to high shear stress are protected [76, 77]. Pro-inflammatory activation of EC is reduced at high shear sites compared to low shear regions, thus providing a potential explanation for the distinct spatial localisation of lesions [70, 78, 79]. Our findings revealed that high shear stress at atheroprotected sites reduced key measures of EC inflammatory activation, p38 MAP kinase activation and VCAM-1 expression, by activating Nrf2 [70] (Fig. 2). By contrast, EC at a low shear, atherosusceptible site contained inactive (cytoplasmic) Nrf2 and were prone to pro-inflammatory activation. We therefore examined whether pharmacological activation of Nrf2 using sulforaphane would suppress inflammation at susceptible sites. In cultured EC, sulforaphane suppressed p38 activation, VCAM-1 expression and ROS production via Nrf2 [70, 71]. Similarly, sulforaphane suppressed p38 activation and VCAM-1 expression at atherosusceptible sites in wild-type but not in Nrf2-/- mice, indicating that the anti-inflammatory effects of sulforaphane were Nrf2-dependent [70] (Fig. 2). Thus our observations reveal that inflammation at atherosusceptible regions can be prevented by sulforaphane-mediated activation of Nrf2.Fig. 2

Bottom Line: Oxidation of low-density lipoproteins (LDL) promotes atherosclerosis by enhancing vascular inflammation and foam cell formation.This review focuses on sulforaphane, an isothiocyanate derived from green vegetables, which induces multiple anti-oxidant enzymes via activation of a transcription factor called Nrf2.A deeper understanding of vascular responses to sulforaphane may inform nutritional approaches to prevent vascular inflammation and atherosclerosis.

View Article: PubMed Central - PubMed

Affiliation: British Heart Foundation, Cardiovascular Sciences Unit, National Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London, W12 ONN UK.

ABSTRACT
Oxidation of low-density lipoproteins (LDL) promotes atherosclerosis by enhancing vascular inflammation and foam cell formation. The corollary is that diets that stimulate endogenous anti-oxidants may protect against atherosclerosis. This review focuses on sulforaphane, an isothiocyanate derived from green vegetables, which induces multiple anti-oxidant enzymes via activation of a transcription factor called Nrf2. Although studies of cultured cells and experimental animals revealed that sulforaphane can suppress inflammatory activation of vascular cells, the potential beneficial effects of sulforaphane in atherosclerosis have not been studied directly. A deeper understanding of vascular responses to sulforaphane may inform nutritional approaches to prevent vascular inflammation and atherosclerosis.

No MeSH data available.


Related in: MedlinePlus