New research from the Johns Hopkins Medical School in the US suggests that broccoli could help people with chronic lung disease.
The findings, published in the American Journal of Respiratory and Critical Care Medicine, focused on chronic obstructive pulmonary disease (COPD), which is considered to be the fourth leading cause of death in the US.
Dr Shyam Biswal led the research and found that the severity of COPD in smokers is linked to lower concentrations of NRF2-dependant antioxidants, which are key components of the lung’s defence system against inflammatory injury.
Broccoli has already been found to help prevent the degradation of NRF2, and could form the basis of new research to further examine its link with lung health.
The key to the vegetable’s protective effects is the naturally occurring sulforaphane.
Sulforapane has been shown to be able to restore antioxidant gene expression in human epithelial tissue in which DJ-1 has been reduced. DJ-1 is a biochemical regulator that stabilizes NRF2, while KEAP1 - another regulator - inhibits NRF2.
Isothicyanate compounds such as that found in broccoli inhibit KEAP1, and thus prevent it from degrading NRF2, according to Dr Peter Barnes, of the National Heart and Lung Institute in London, who wrote an accompanying editorial in the American journal.
He wrote: “While clinical trials to date of antioxidants have been disappointing in improving the clinical course of patients with COPD, this study points to a possibility of benefit from restoring NRF2 levels in damaged lungs by reducing the action of KEAP1, which is an inhibitor of NRF2.
“Increasing NRF2 may also restore important detoxifying enzymes to counteract other effects of tobacco smoke. This has been achieved in vitro and in vivo by isothiocynate compounds, such as sulforaphane, which occurs naturally in broccoli and [wasabi].”
In the current study, researchers examined tissue samples from the lungs of smokers with and without COPD to determine if there were differences in measured levels of NRF2 expression and the level of KEAP1 and DJ-1.
The lungs of patients with COPD showed markedly decreased levels of NRF2-dependent antioxidants and increased oxidative stress markers, compared to non-COPD lungs.
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