Abstract
BackgroundExposure to carbon black nanoparticles (CBNPs), a well-known industrial production, promotes pulmonary toxicity through inflammation and oxidative stress. Recent studies show that some polyphenols exert their antioxidant properties through regulation of protein kinase C-α (PKC-α) and NADPH oxidase (Nox) signaling. Resveratrol, a dietary polyphenol in fruits, possesses various health beneficial effects including anti-inflammatory and antioxidative properties. In this study, we aimed to elucidate the involvement of PKC-α and Nox in CBNPs-induced inflammation and oxidative stress, and to investigate the protective effects of resveratrol on CBNP-induced inflammation and oxidative stress in human lung epithelial A549 cells.MethodsThe production of reactive oxygen species (ROS) and the change of mitochondrial membrane potential (ΔΨm) were measured by flow cytometry. Nitric oxide (NO) was measured using the Griess reagent, and prostaglandin E2 (PGE2) production was detected by ELISA, while protein expressions were measured by Western blotting analysis.ResultsIn lung epithelial A549 cells, CBNPs significantly enhanced oxidative stress by upregulation of Nox2 and membrane expression of p67phox accompanied with increase of ROS production. CBNPs also increased inflammatory factors, including iNOS, COX-2, NO and PGE2. However, resveratrol attenuated the above effects induced by CBNPs in A549 cells; additionally, CBNPs-induced activation of PKC-α was observed. We found that PKC-α inhibitor (Gö6976) could attenuate CBNPs-induced inflammation by down-regulation of ROS, NO and PGE2 production in A549 cells, suggesting PKC-α might be involved in CBNPs-induced oxidative stress and inflammation. Our results also found resveratrol was able to inhibit protein expression of PKC-α induced by CBNPs. Moreover, ROS scavenger (NAC) and Nox inhibitor (DPI) attenuated CBNPs-induced expressions of iNOS and COX-2. DPI could also attenuate CBNPs-induced ROS, NO and PGE2 production.ConclusionsResveratrol attenuated CBNPs-induced oxidative and inflammatory factors in lung epithelial A549 cells, at least in part via inhibiting PKC-α- and Nox-related signaling.
Highlights
Exposure to carbon black nanoparticles (CBNPs), a well-known industrial production, promotes pulmonary toxicity through inflammation and oxidative stress
Lung epithelial cells in the respiratory tract are the first barrier in contact with these inhalable NPs, and A549 human lung epithelial cells have been wildly used for studying NPs-induced cytotoxicity [21,22,23]; in this study, we further investigated the role of protein kinase C-α (PKC-α) and NADPH oxidase (Nox) activation in CBNPs-induced inflammation on A549 cells
CBNPs decrease cell viability with loss of mitochondrial membrane potential (ΔΨm) and increase of nuclear condensation in A549 cells To examine the cytotoxic effects of CBNPs on lung epithelial cells, cultured A549 were treated with various concentrations of CBNPs for 24 h
Summary
Exposure to carbon black nanoparticles (CBNPs), a well-known industrial production, promotes pulmonary toxicity through inflammation and oxidative stress. We aimed to elucidate the involvement of PKC-α and Nox in CBNPs-induced inflammation and oxidative stress, and to investigate the protective effects of resveratrol on CBNP-induced inflammation and oxidative stress in human lung epithelial A549 cells. The NPs can enter the lungs during respiration due to their tiny size with a diameter less than 100 nm [2], subsequently inducing apoptosis and pro-inflammatory reaction in lung epithelial cells [3]. Exposure to CBNPs is known to induce lung inflammation in vivo [10, 11], and possesses the potential to generate reactive oxygen species (ROS) and inflammatory factors [12,13,14,15,16]. ERK MAP kinase and p38 MAP kinase might be involved in CBNPs-induced ROS production in alveolar macrophage [12]
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