Cerium Oxide Nanoparticles Inhibits Oxidative Stress and Nuclear Factor-κB Activation in H9c2 Cardiomyocytes Exposed to Cigarette Smoke Extract

Abstract

Cigarette smoke contains and generates a large amount of reactive oxygen species (ROS) that affect normal cellular function and have pathogenic consequences in the cardiovascular system. Increased oxidative stress and inflammation are considered to be an important mechanism of cardiovascular injury induced by cigarette smoke. Antioxidants may serve as effective therapeutic agents against smoke-related cardiovascular disease. Because of the presence of oxygen vacancies on its surface and self-regenerative cycle of its dual oxidation states, Ce 3ϩ and Ce 4ϩ , cerium oxide (CeO 2 ) nanoparticles offer a potential to quench ROS in biological systems. In this study, we determined the ability of CeO 2 nanoparticles to protect against cigarette smoke extract (CSE)-induced oxidative stress and inflammation in cultured rat H9c2 cardiomyocytes. CeO 2 nanoparticles pretreatment of H9c2 cells resulted in significant inhibition of CSE-induced ROS production and cell death. Pretreatment of H9c2 cells with CeO 2 nanoparticles suppressed CSEinduced phosphorylation of IB␣, nuclear translocation of p65 subunit of nuclear factor-B (NF-B), and NF-B reporter activity in H9c2 cells. CeO 2 nanoparticles pretreatment also resulted in a significant down-regulation of NF-B-regulated inflammatory genes tumor necrosis factor-␣, interleukin (IL)-1␤, IL-6, and inducible nitric-oxide synthase and further inhibited CSE-induced depletion of antioxidant enzymes, such as copper zinc superoxide dismutase, manganese superoxide dismutase, and intracellular glutathione content. These results indicate that CeO 2 nanoparticles can inhibit CSE-induced cell damage via inhibition of ROS generation, NF-B activation, inflammatory gene expression, and antioxidant depletion and may have a great potential for treatment of smoking-related diseases.

Short-Term Nose-Only Water-Pipe (Shisha) Smoking Exposure Accelerates Coagulation and Causes Cardiac Inflammation and Oxidative Stress in Mice

“…Similar findings were observed in mice exposed to WPS for 1 month [14]. In cultured rat H9c2 cardiomyocytes, CS extract was found to cause upregulation of NF-κB-regulated inflammatory genes TNFα, IL-6 and IL-1β and to induce depletion of antioxidant enzymes [37]. It remains to determine if there is any selectivity of WPS components to specific heart compartments leading to a differential proinflammatory and procoagulatory effects.…”

Cerium dioxide nanoparticles do not modulate the lipopolysaccharide-induced inflammatory response in human monocytes

“…23 Moreover, CeO 2 nanoparticles have been reported to reduce oxidative signaling and cell death induced by cigarette smoke, diesel exhaust, and hydrogen peroxide. [24][25][26] In contrast, other in vitro and in vivo experiments suggest that CeO 2 nanoparticles produce inflammation, reactive oxygen species, lipid peroxidation, liver and lung damage, acute and chronic fibrotic effects, and altered macrophage phenotypes. [27][28][29][30][31] Variation in target species/ cell type, experimental design (exposure concentration and duration) and nanoparticle characteristics (shape, size, purity, Figure 1, stained with propidium iodide and analyzed using flow cytometry.…”

Toxicity and Protective Effects of Cerium Oxide Nanoparticles (Nanoceria) Depending on Their Preparation Method, Particle Size, Cell Type, and Exposure Route

“…[20] This leads to the protection of eukaryotic cells against oxidative stress, as it was previously reported in many studies. [21,22] Niu et al [23] and Korsvik et al [24] have proposed a mechanism, shown in Equations (2) and (3), by which ceria can scavenge radicals thanks to its redox potential.…”