Resveratrol relieves particulate matter (mean diameter < 2.5 μm)-induced oxidative injury of lung cells through attenuation of autophagy deregulation.

Oxidative stress and inflammation are critically implicated in ambient fine particulate matter (mean diameter < 2.5 μm; PM2.5 )-induced lung injury. Autophagy, playing a crucial role in various physiopathological conditions, modulates cellular homeostasis and stress adaptation. Resveratrol is a phytoalexin that exerts potent antioxidant effects on cardiopulmonary diseases. To date, the mechanisms by which resveratrol protects against PM2.5 remain to be elucidated. In the present study, we investigated the effect of resveratrol on PM2.5 -induced oxidative injury. The potential role of nuclear factor erythroid-2-related factor 2 and autophagy in this progress was explored. Human bronchial epithelial cells were treated with PM2.5 and the cytotoxicity and oxidative stress markers were determined. The results showed that PM2.5 decreased cell viability and elevated the level of lactate dehydrogenase. The levels of malondialdehyde and reactive oxygen species were increased by PM2.5 exposure. PM2.5 also induced a significant increase of the inflammatory cytokines including interleukin (IL)-6, IL-8, IL-1β and tumor necrosis factor α. Meanwhile, PM2.5 triggered autophagy formation and alteration of the nuclear factor erythroid-2-related factor 2 pathway. Furthermore, human bronchial epithelial cells were co-treated with PM2.5 and resveratrol in the presence or absence of 3-methylamphetamine, an inhibitor of autophagic formation. It was revealed that resveratrol intervention abolished PM2.5 -induced oxidative injury partially through the suppression of autophagy deregulation. Findings from this study could provide new insights into the molecular mechanisms of pulmonary intervention during PM2.5 exposure.