Through the use of a molecule similar to one found in an experimental cancer drug, researchers found that activation of a key component of the lung’s antioxidant defense system, Nrf2, can prevent emphysema in mice.
During the study, the researchers observed mice exposed to cigarette smoke to determine if activation of Nrf2 could prevent emphysema. Exposed mice—fed a diet containing CDDO-Im, which is known to activate Nrf2—were significantly less likely to have oxidative stress and lung cell damage associated with emphysema. The researchers from Johns Hopkins Bloomberg School of Public Health believe that activation of Nrf2 could be a novel target for therapies to prevent chronic obstructive pulmonary disease (COPD).
“Targeting the Nrf2 pathway presents a novel strategy which needs to be tested for their efficacy in intervening COPD in patients,” says senior author Shyam Biswal, PhD, associate professor in the Bloomberg School of Public Health.
Nrf2 (nuclear factor erythroid-derived 2-related factor 2) works as a “master gene” that turns on numerous antioxidant and pollutant-detoxifying genes to protect the lungs from environmental pollutants, such as cigarette smoke.
“Nrf2 is an important regulator of the body’s antioxidant defense system, and activation of Nrf2 is a promising therapeutic strategy for attenuating COPD progression in patients,” says lead author Thomas Sussan, PhD.
The study is published in the online Early Edition of PNAS: Proceeding of the National Academy of Sciences.
