Broccoli compound may combat COPD

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In chronic obstructive pulmonary disease (COPD), damage to immune cells limits the lungs’ ability to fight off bacterial infections. According to a new study, boosting the activity of a specific molecule in these cells can restore their defensive powers. In patients with COPD, immune cells called macrophages lose their ability to engulf and remove bacteria, making the lungs more vulnerable to infection. Until now, no one knew how to reverse this damage to the macrophages.

A team of scientists at Johns Hopkins University, led by Drs. Shyam Biswal and Robert Wise, investigated why macrophages don’t work properly in COPD patients. Previous research suggested that a process called oxidative stress might be to blame. Oxidative stress occurs when the body can’t effectively neutralize damaging compounds called peroxides and free radicals.

A molecule called Nrf2 can cause cells to make more antioxidants, which neutralize these harmful compounds. Previous studies found reduced Nrf2 activity in severe COPD. The scientists suspected that increasing Nrf2 activity might restore the ability of macrophages to remove bacteria. To test their theory, the team used a chemical called sulforaphane, which is known to activate Nrf2. A precursor of sulforaphane is found in broccoli. The research was cosponsored by NIH’s National Heart, Lung and Blood Institute (NHLBI) and National Institute of Environmental Health Sciences (NIEHS). The results appeared in the April 13, 2011, issue of Science Translational Medicine.

The researchers first took macrophages from the lungs of patients with moderate COPD. When they treated these macrophages with sulforaphane, they saw higher Nrf2 levels in the cells. Sulforaphane treatment also boosted the ability of cultured macrophages to clear 2 of the major types of bacteria that infect COPD patients. Macrophage uptake of bacteria rose 300% after treatment, whether the cells came from smokers or non–smokers. Experiments in mouse and human cells revealed that sulforaphane, through Nrf2, increases levels of a receptor called MARCO on macrophages. MARCO activity was necessary for macrophages to engulf bacteria after sulforaphane treatment. Mice exposed to smoke had lower levels of MARCO. Furthermore, smoke-exposed mice genetically engineered to lack Nrf2 had more lung inflammation and higher levels of bacteria.

The team gave sulforaphane with a nebulizer to mice exposed to smoke and found that the mice’s lungs showed reduced inflammation and bacterial burden. The researchers also gave human COPD patients broccoli sprout extract enriched with sulforaphane for 2 weeks. The patients taking the extract had higher levels of MARCO and Nrf2–controlled antioxidants in their blood cells. A NHLBI–sponsored clinical trial is now being conducted to test if sulforaphane can provide relief to patients with COPD. (Source NIH)
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Cilostazol for prevention of ischemic stroke

The antiplatelet agent cilostazol is a phosphodiesterase 3 inhibitor that is used mainly to treat intermittent claudication in patients with peripheral artery disease. Several controlled trials in Asia have found that cilostazol is effective for the secondary prevention of cerebral infarction.

In the largest such trial (CSPS II), cilostazol (100 mg twice daily) was not inferior to aspirin (81 mg daily) in preventing recurrent stroke (infarction or hemorrhage) at a mean follow–up of 29 months in 2757 patients in Japan with a recent noncardioembolic cerebral infarction.

Dr KK Aggarwal
Editor in Chief

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