14 September 2009
How greens may protect the heart
Researchers have discovered a possible reason why green vegetables such as broccoli, cabbage and cauliflower are good for the heart.
Their work suggests a chemical found in the vegetables can boost a natural defence mechanism to protect arteries from disease.
The Imperial College London team hope their work could lead to new dietary treatments to prevent heart problems.
Much heart disease is caused by the build up of fatty plaques in the arteries known as atherosclerosis.
However, arteries do not get clogged up with these plaques in a uniform way.
Bends and branches of blood vessels - where blood flow is disrupted and can be sluggish - are much more prone to the build-up.
The latest study has shown that a protein that usually protects against plaque build up called Nrf2 is inactive in areas of arteries that are prone to disease.
However, it also found that treatment with a chemical found in green "brassica" vegetables such as broccoli can activate Nrf2 in these disease-prone regions.
Lead researcher Dr Paul Evans said: "We found that the innermost layer of cells at branches and bends of arteries lack the active form of Nrf2, which may explain why they are prone to inflammation and disease.
"Treatment with the natural compound sulforaphane reduced inflammation at the high-risk areas by 'switching on' Nrf2.
"Sulforaphane is found naturally in broccoli, so our next steps include testing whether simply eating broccoli, or other vegetables in their 'family', has the same protective effect.
"We also need to see if the compound can reduce the progression of disease in affected arteries."
Professor Peter Weissberg, medical director of the British Heart Foundation, which funded the research, said: "These fascinating findings provide a possible mechanism by which eating vegetables protects against heart disease.
"As well as adding evidence to support the importance of eating 'five-a-day', the biochemistry revealed in this research could lead to more targeted dietary or medical approaches to prevent or lessen disease that leads to heart attacks and strokes."
Using normal mice, and mice engineered to lack the Nrf2 protein, the research found that in straight sections of arteries Nrf2 was present in the endothelial 'lining' cells.
Through its action on other proteins, it prevented the cells from becoming inflamed, an early stage in the development of atherosclerosis.
In the lining cells of disease-prone sites - such as bending or branched arteries - Nrf2 was attached to a protein that made it inactive. This stifled its protective properties.
But the addition of sulforaphane re-activated Nrf2 in the disease-prone regions of the artery, restoring the cells' ability to protect themselves from becoming inflamed.
The researchers believe that this will enable these artery regions to remain healthy for longer, or even reduce the progression of existing disease.