Naringenin is found mainly in citrus fruits, and is thought to be beneficial in the prevention and control of
lung diseases. This study aims to investigate the mechanisms of
naringenin against the damage in the lung caused by cigarette
smoke. A system bioinformatic approach was proposed to predict the mechanisms of
naringenin for protecting lung health. Then, we validated this prediction in BEAS-2B cells treated with cigarette
smoke extract (CSE). System bioinformatic analysis indicated that
naringenin exhibits protective effects on lung through the inhibition of
inflammation and suppression of oxidative stress based on a multi-pathways network, mainly including oxidative stress pathway, Nrf2 pathway, Lung
fibrosis pathway,
IL-3 signaling pathway, and
Aryl hydrocarbon receptor pathway. The in vitro results showed that
naringenin significantly attenuated CSE-induced up-regulation of
IL-8 and TNF-α. CSE stimulation increased the
mRNA expressions of Nrf2, HO-1, and NQO1; the levels of total
protein and
nuclear protein of Nrf2; and the activity of SOD on days 2 and 4; but decreased these indexes on day 6.
Naringenin can balance the
antioxidant system by regulating Nrf2 and its downstream genes, preliminarily validating that Nrf2 pathway is involved in the protection offered by
naringenin against cigarette
smoke-induced damage to the lung. It suggests that dietary
naringenin shows possible potential use in the management of lung health.