http://www.sciencedaily.com/releases/2011/10/111017124251.htmBroccoli-Based Compound Beats Drug Resistance in Lung Disease
ScienceDaily (Oct. 17, 2011) — Chronic obstructive pulmonary disease (COPD) is a common lung disease that gets progressively worse over time, making it harder and harder to breathe. It is caused primarily by cigarette smoking, which leads to persistent inflammation in the airways and the subsequent destruction of the lung tissue.
Given the central role of inflammation in COPD, it is surprising that patients derive little benefit from treatment with potent anti-inflammatory drugs known as corticosteroids.
Working with cells from individuals with COPD, a team of researchers led by Shyam Biswal and Rajesh Thimmulappa, at Johns Hopkins University, Baltimore, has identified a candidate therapeutic that could potentially be used to augment the anti-inflammatory effects of corticosteroids in individuals with COPD -- sulforaphane, a compound obtained from cruciferous vegetables such as broccoli, Brussels sprouts, and cabbages.
http://www.lef.org/whatshot/2011_10.htm#Broccoli-compound-improves-steroid-response-in-COPD-patientsBroccoli compound improves steroid response in COPD patients
Large analysis links exercise with reduced mortality over a decadeOctober 24 2011. An article published online on October 17, 2011 in the Journal of Clinical Investigation revealed that sulforaphane, a compound that occurs in broccoli and other cruciferous vegetables, improves sensitivity to corticosteroid drugs used to treat chronic obstructive pulmonary disease (COPD), a disease that is mainly result of smoking, characterized by chronic bronchitis and emphysema. The disease is currently treated with corticosteroids, however, the drugs only reduce symptoms by approximately 20 percent.
Individuals diagnosed with COPD experience a reduction in their lungs of histone deacetylase 2 (HDAC2), a substance that is essential to the anti-inflammatory pathway initiated by steroid drugs. In the current research, a team from Johns Hopkins University discovered that S-nitrosylation of HCAC2 due to cigarette smoke exposure resulted in HDAC2 dysfunction in lung macrophages derived from individuals with COPD. "This study provides the mechanism of exaggerated inflammation observed in COPD patients during exacerbations, which has been a barrier to developing effective therapy," stated coauthor Rajesh Thimmulappa, PhD, who is an assistant scientist at Johns Hopkins Bloomberg School of Medicine's Department of Environmental Health Sciences.
It was further discovered that sulforaphane denitrosylates HDAC2, which restored corticosteroid sensitivity. In previous research, the team demonstrated that sulforaphane activates a pathway known as Nrf2. "Restoring corticosteroid sensitivity in patients with COPD by targeting the Nrf2 pathway holds promise for effectively treating exacerbations," noted senior author Shyam Biswal, PhD, who is a professor at the Bloomberg School of Medicine's Department of Environmental Health Sciences and Division of Pulmonary and Critical Care Medicine.
"Nrf2 activators such as sulforaphane can counteract oxidative and nitrosative stress and mediate glutathione-dependent denitrosylation, thereby restoring HDAC2 activity," the authors write. "The small-molecule Nrf2 activator sulforaphane may be useful as an adjuvant therapy to augment the antiinflammatory effects of glucocorticosteroids in COPD and other inflammatory diseases."
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