According to a new study on the properties of broccoli, eating the vegetable may offer protection from heart disease.
Broccoli is a member of the cabbage family, or Brassicaceae/Cruciferae and has abundant fleshy flower heads, which are usually green in colour and arranged tree-like on branches which sprout from a thick, edible stalk.
Broccoli was originally an Italian vegetable and is a cool-weather crop that does poorly in hot summer weather.
In recent years broccoli has been found to be an excellent source of antioxidants, vitamins and fiber that may protect against a variety of cancers, and other studies too have also suggested that broccoli may benefit the heart.
Dipak K. Das and colleagues at the Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, tested that claim in a study with rats, resulting in impressive new evidence.
The rats were fed broccoli extract for a one month period and the effects on the rats' heart muscle were measured and compared to a control group that ate a regular diet.
The researchers found that the broccoli-fed animals had improved heart function and less heart muscle damage when deprived of oxygen compared to the control group.
They believe broccoli's heart-healthy effects are because of its high concentrations of certain substances that appear to boost levels of a heart-protective protein called thioredoxin.
The researchers say there is abundant epidemiological evidence which indicates the health benefits of eating broccoli and it also contains high amounts of selenium and glucosinolates which help produce the cardioprotective protein thioredoxin (Trx).
The researchers say the broccoli diet resulted in significant cardio protection.
The study is published this week in the Journal of Agricultural and Food Chemistry.
Sure enough, the mice that received the visceral fat transplants developed atherosclerosis at a much-accelerated rate, and experienced the same type of inflammation as the leptin-deficient mice had. Meanwhile, those that received subcutaneous fat did not experience an increase in atherosclerosis despite having increased inflammation. The mice that had the sham operations developed neither inflammation nor increased atherosclerosis.
There appeared to be an interaction between the macrophages causing the inflammation in the visceral fat, and the process of atherosclerosis, says Eitzman, who notes that blood vessels far from the site of the fat transplant developed increased atherosclerosis.
Finally, the team attempted to calm the inflammation and curb the atherosclerosis by treating the mice with pioglitazone “ a member of the class of drugs called thiazolidinediones or TZDs that are often used to treat diabetes. While TZD drugs have an impact on metabolism, which makes them useful in diabetes, they also have been discovered to have an anti-inflammatory effect.
And in fact, the drug reduced both the concentration of macrophages and MCP-1, and atherosclerosis, in those mice that received transplants of visceral fat. But the drug had no effect in the other mice.
Now that they have demonstrated the linkage between belly fat, inflammation and hardened arteries, and a potential mechanism for reversing the phenomenon, the team is working on new pieces of the puzzle. Specifically, they're looking for the factors that might trigger macrophages to invade the area and bring on inflammation, and for blood-borne molecules called biomarkers that might be used as a way to identify early warning signs of atherosclerosis. They'll also look at other classes of drugs to see if they might have a protective effect, because TZD drugs act on many systems and cause some side effects.
In addition to Eitzman, ?–hman and Lawrence, the team includes former research associate Yuechen Shen, M.D., former U-M undergraduate Chinyere Obimba, B.S., now a Harvard Medical School student; former U-M undergraduate and current U-M medical student Andrew P. Wright, B.S.; and Mark Warnock, B.S. The research was funded by the National Heart, Lung and Blood Institute.
med.umich/