Quercetin protects against pulmonary oxidant stress via heme oxygenase-1 induction in lung epithelial cells

The lung is a primary target for oxygen toxicity because of its constant exposure to high oxygen levels and environmental oxidants. Quercetin is one of the most commonly found dietary flavonoids, and it provides cytoprotective actions via activation of specific transcriptional factors and upregulation of endogenous defensive pathways. In the present study, we showed that quercetin increased the levels of heme oxygenase (HO)-1 expression and protected against hydrogen peroxide (H2O2)-induced cytotoxicity in lung epithelial cell lines. Quercetin suppressed H2O2-induced apoptotic events, including hypodiploid cells, activation of caspase 3 enzyme activity and lactate dehydrogenase release. This cytoprotective effect was attenuated by the addition of the HO inhibitor, tin protoporphyrin IX. In addition, the end products of heme metabolites catalyzed by HO-1, carbon monoxide and bilirubin, protect against H2O2-induced cytotoxicity in LA-4 cells. Quercetin may well be one of the promising substances to attenuate oxidative epithelial cell injury in lung inflammation.

► Quercetin protected alveolar epithelial cells from H2O2-induced cell death.
► Quercetin increased the levels of heme oxygenase (HO)-1 expression.
► Quercetin-induced cytoprotective effects were mediated through Nrf2-HO-1 pathway.