RESUMEN
Copper nanoparticles (Cu NPs) show promise in dentistry for combating bacterial dysbiosis and tooth decay. Understanding their effects on commensal versus pathogenic bacteria is vital for maintaining oral health balance. While Cu NPs demonstrate antibacterial properties against various oral bacteria, including common pathogens associated with tooth decay, their impact on commensal bacteria requires careful examination. In our work, we analyzed three types of Cu NPs for their effects on the growth, viability, and biofilm formation of representative caries-associated and commensal oral bacteria. S. sanguinis showed high tolerance to all Cu NPs, while L. rhamnosus was highly sensitive. Oxide-Cu NPs exhibited a stronger inhibitory effect on pathobionts compared with commensal bacteria. Moreover, the biofilm formation of the key cariogenic bacteria S. mutans was reduced, with minimal negative effects on commensal species' biofilm formation. All our results showed that CuO nanoparticles (CuO NPs) exhibit reduced toxicity toward commensal bacteria growth and development but have a strong impact on pathogens. This suggests their potential for targeted treatments against pathogenic bacteria, which could help in maintaining the balance of the oral bacterial community.
RESUMEN
Cyclooxygenase-2 (COX-2) is constitutively expressed and highly regulated in the thick ascending limb (TAL). As COX-2 inhibitors (Coxibs) increase COX-2 expression, we tested the hypothesis that a negative feedback mechanism involving PGE(2) EP3 receptors regulates COX-2 expression in the TAL. Sprague-Dawley rats were treated with a Coxib [celecoxib (20 mg·kg(-1)·day(-1)) or rofecoxib (10 mg·kg(-1)·day(-1))], with or without sulprostone (20 µg·kg(-1)·day(-1)). Sulprostone was given using two protocols, namely, previous to Coxib treatment (prevention effect; Sulp7-Coxib5 group) and 5 days after initiation of Coxib treatment (regression effect; Coxib10-Sulp5 group). Immunohistochemical and morphometric analysis revealed that the stained area for COX-2-positive TAL cells (µm(2)/field) increased in Coxib-treated rats (Sham: 412 ± 56.3, Coxib: 794 ± 153.3). The Coxib effect was inhibited when sulprostone was used in either the prevention (285 ± 56.9) or regression (345 ± 51.1) protocols. Western blot analysis revealed a 2.1 ± 0.3-fold increase in COX-2 protein expression in the Coxib-treated group, an effect abolished by sulprostone using either the prevention (1.2 ± 0.3-fold) or regression (0.6 ± 0.4-fold vs. control, P < 0.05) protocols. Similarly, the 6.4 ± 0.6-fold increase in COX-2 mRNA abundance induced by Coxibs (P < 0.05) was inhibited by sulprostone; prevention: 0.9 ± 0.3-fold (P < 0.05) and regression: 0.6 ± 0.1 (P < 0.05). Administration of a selective EP3 receptor antagonist, L-798106, also increased the area for COX-2-stained cells, COX-2 mRNA accumulation, and protein expression in the TAL. Collectively, the data suggest that COX-2 levels are regulated by a novel negative feedback loop mediated by PGE(2) acting on its EP3 receptor in the TAL.