ブロッコリが糖尿病性血管障害を回復させる可能性

 ブロッコリが糖尿病性心血管障害を回復させる可能性があるとの研究報告。
 野菜で発見された sulforaphane という化合物が鍵を握っている。血管を保護する酵素の生産を促し、重要な細胞障害を起こす分子の上昇を抑える作用がある。
 ブロッコリなどのアブラナ属野菜は以前から心臓発作と卒中のより低いリスクと関連ありといわれている。
 糖尿病を持つ人々は、最高で5倍も心臓発作と卒中などの心血管疾患になりやすく、両者は血管損傷と関連している。
 高血糖によって損われた血管細胞へのsulforaphaneの効果をテストしたところ、高血糖だと Reactive Oxygen Species(ROS)と呼ばれる体内分子レベルが3倍となり細胞損傷をきたすのだが、ROS の73%の低下がみられた。。
 また、sulforaphaneが体内で、防御能のある抗酸化剤と無毒化酵素を活性化し損傷から細胞と組織を保護する作用のある nrf2 と呼ばれる蛋白質を活性化するとわかった。
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ブロッコリが心臓病に有効
http://kurie.at.webry.info/200801/article_46.html
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Page last updated at 23:12 GMT, Tuesday, 5 August 2008 00:12 UK
Broccoli may undo diabetes damage
http://news.bbc.co.uk/2/hi/health/7541639.stm

画像Broccoli
Broccoli may help ward off prostate cancer

Eating broccoli could reverse the damage caused by diabetes to heart blood vessels, research suggests.

A University of Warwick team believe the key is a compound found in the vegetable, called sulforaphane.

It encourages production of enzymes which protect the blood vessels, and a reduction in high levels of molecules which cause significant cell damage.

Brassica vegetables such as broccoli have previously been linked to a lower risk of heart attacks and strokes.


Our study suggests that compounds such as sulforaphane from broccoli may help counter processes linked to the development of vascular disease in diabetes
Professor Paul Thornalley
University of Warwick

People with diabetes are up to five times more likely to develop cardiovascular diseases such as heart attacks and strokes; both are linked to damaged blood vessels.

The Warwick team, whose work is reported in the journal Diabetes, tested the effects of sulforaphane on blood vessel cells damaged by high glucose levels (hyperglycaemia), which are associated with diabetes.

They recorded a 73% reduction of molecules in the body called Reactive Oxygen Species (ROS).

Hyperglycaemia can cause levels of ROS to increase three-fold and such high levels can damage human cells.

The researchers also found that sulforaphane activated a protein in the body called nrf2, which protects cells and tissues from damage by activating protective antioxidant and detoxifying enzymes.

Countering vascular disease

Lead researcher Professor Paul Thornalley said: "Our study suggests that compounds such as sulforaphane from broccoli may help counter processes linked to the development of vascular disease in diabetes.

"In future, it will be important to test if eating a diet rich in brassica vegetables has health benefits for diabetic patients. We expect that it will."

Dr Iain Frame, director of research at the charity Diabetes UK, stressed that research carried out on cells in the lab was a long way from the real life situation.

However, he said: "It is encouraging to see that Professor Thornalley and his team have identified a potentially important substance that may protect and repair blood vessels from the damaging effects of diabetes.

"It also may help add some scientific weight to the argument that eating broccoli is good for you."

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Diabetes Publish Ahead of Print published online ahead of print July 15, 2008
DOI: 10.2337/db06-1003

Original Research
Activation of NF-E2-related factor-2 reverses biochemical dysfunction of endothelial cells induced by hyperglycemia linked to vascular disease


Mingzhan Xue1, Qingwen Qian2, Adaikalakoteswari Antonysunil1, Naila Rabbani1,2, Roya Babaei-Jadidi2, and Paul J. Thornalley1,2

1Clinical Sciences Research Institute, Warwick Medical School, University of Warwick, University Hospital, Coventry CV2 2DX, U.K. and
2Department of Biological Sciences, University of Essex, Central Campus, Wivenhoe Park, Colchester, Essex CO4 3SQ, U.K.

OBJECTIVE–: Sulforaphane (SFN) is an activator of transcription factor NF-E2-related factor-2 (nrf2) that regulates gene expression through the promoter antioxidant response element (ARE). Nrf2 regulates the transcription of a battery of protective and metabolic enzymes. The aim of this study was to assess if activation of nrf2 by SFN in human microvascular endothelial cells prevents metabolic dysfunction in hyperglycemia.

RESEARCH DESIGN AND METHODS–: Human microvascular HMEC-1 endothelial cells were incubated in low and high glucose concentrations (5 and 30 mM) and activation of nrf2 assessed by nuclear translocation. The effect of SFN on multiple pathways of biochemical dysfunction, increased reactive oxygen species (ROS) formation, hexosamine pathway, protein kinase C pathway and increased formation of methylglyoxal, was assessed.

RESULTS–: Activation of nrf2 by SFN induced nuclear translocation of nrf2 and increased ARE-linked gene expression. For example, 3 - 5 fold increased expression of transketolase and glutathione reductase. Hyperglycemia increased the formation of ROS – an effect linked to mitochondrial dysfunction and prevented by SFN. ROS formation was increased further by knockdown of nrf2 and transketolase expression. This also abolished the counteracting effect of SFN, suggesting mediation by nrf2 and related increase of transketolase expression. SFN also prevented hyperglycemia-induced activation of the hexosamine and protein kinase C pathways, and prevented increased cellular accumulation and excretion of the glycating agent, methylglyoxal.

CONCLUSION–: We conclude that activation of nrf2 may prevent biochemical dysfunction and related functional responses of endothelial cells induced by hyperglycemia in which increased expression of transketolase has a pivotal role.

Correspondence: P.J.Thornalley@warwick.ac.uk

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