hCeO2@ Cu5.4O nanoparticle alleviates inflammatory responses by regulating the CTSB–NLRP3 signaling pathway

Abstract

Inflammatory responses, especially chronic inflammation, are closely associated with many systemic diseases. There are many ways to treat and alleviate inflammation, but how to solve this problem at the molecular level has always been a hot topic in research. The use of nanoparticles (NPs) as anti-inflammatory agents is a potential treatment method. We synthesized new hollow cerium oxide nanomaterials (hCeO2 NPs) doped with different concentrations of Cu5.4O NPs [the molar ratio of Cu/(Ce + Cu) was 50%, 67%, and 83%, respectively], characterized their surface morphology and physicochemical properties, and screened the safe concentration of hCeO2@Cu5.4O using the CCK8 method. Macrophages were cultured, and P.g-lipopolysaccharide-stimulated was used as a model of inflammation and co-cultured with hCeO2@Cu5.4O NPs. We then observe the effect of the transcription levels of CTSB, NLRP3, caspase-1, ASC, IL-18, and IL-1β by PCR and detect its effect on the expression level of CTSB protein by Western blot. The levels of IL-18 and IL-1β in the cell supernatant were measured by enzyme-linked immunosorbent assay. Our results indicated that hCeO2@Cu5.4O NPs could reduce the production of reactive oxygen species and inhibit CTSB and NLRP3 to alleviate the damage caused by the inflammatory response to cells. More importantly, hCeO2@Cu5.4O NPs showed stronger anti-inflammatory effects as Cu5.4O NP doping increased. Therefore, the development of the novel nanomaterial hCeO2@Cu5.4O NPs provides a possible new approach for the treatment of inflammatory diseases.

Natural Bioactive Compounds in the Management of Periodontal Diseases: A Comprehensive Review

“…CeO 2 nanoparticles further inhibit NF-κB activation, reducing the production of pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 in periodontal tissues. With antioxidant properties, nanoparticles neutralize ROS; for instance, CeO 2 nanoparticles exhibit superoxide dismutase (SOD) and catalase-mimetic activities, directly scavenging superoxide radicals and hydrogen peroxide [79,80]. This reduces oxidative stress in gingival fibroblasts, protecting them from ROS-induced damage [81].…”