RESUMEN
Doping nanoparticles represents a strategy for modulating the energy levels and surface states of nanocrystals (NCs), thereby enhancing their efficiency and mitigating toxicity. Thus, we herein focus on the successful synthesis of pure and gold (Au)-doped zinc oxide (ZnO) nanocrystals (NCs), investigating their physical-chemical properties and evaluating their applicability and toxicity through in vitro and in vivo assessments. The optical, structural, and photocatalytic characteristics of these NCs were scrutinized by using optical absorption (OA), X-ray diffraction (XRD), and methylene blue degradation, respectively. The formation and doping of the NCs were corroborated by the XRD and OA results. While the introduction of Au as a dopant did induce changes in the phase and size of ZnO, a high concentration of Au ions in ZnO led to a reduction in their photocatalytic activity. This demonstrated a restricted antibacterial efficacy against Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus aureus. Remarkably, Au-doped counterparts exhibited enhanced biocompatibility in comparison to ZnO, as evidenced in both in vitro (murine macrophage cells) and in vivo (Drosophila melanogaster) studies. Furthermore, confocal microscopy images showed a high luminescence of Au-doped ZnO NCs in vivo. Thus, this study underscores the potential of Au doping of ZnO NCs as a promising technique to enhance material properties and increase biocompatibility.
RESUMEN
Group B Streptococcus (GBS) infection during pregnancy is involved in maternal sepsis, chorioamnionitis, prematurity, fetal infection, neonatal sepsis, and neurodevelopmental alterations. The GBS-induced chorioamnionitis leads to a plethora of immune and trophoblast cells alterations that could influence endothelial cells to respond differently to angiogenic mediators and alter placental vascular structure and function in pregnant women. In this context, preventive measures are needed to reduce such dysfunctions. As such, we evaluated the effects of a non-lethal exposure to inactivated GBS on trophoblast cells and chorionic villi explants, and if the treatment with uvaol would mitigate these effects. The concentration of 106 CFU of GBS was chosen since it was unable to reduce the HTR-8/SVneo cell line nor term chorionic villi explant viability. Raman spectroscopy of trophoblast cells showed significant alterations in their biochemical signature, mostly reverted by uvaol. GBS exposure increased HTR-8/SVneo cells IL-1ß and IFN-γ production, phagocytosis, oxidative stress, and decreased trophoblast cell migration. The Ea.hy926 endothelial cell line produced angiopoietin-2, CXCL-8, EGF, FGF-b, IL-6, PlGF, sPECAM-1, and VEGF in culture. When co-cultured in invasion assay with HTR-8/SVneo trophoblast cells, the co-culture had increased production of angiopoietin-2, CXCL-8, FGF-b, and VEGF, while reduced sPECAM-1 and IL-6. GBS exposure led to increased CXCL-8 and IL-6 production, both prevented by uvaol. Chorionic villi explants followed the same patterns of production when exposed to GBS and response to uvaol treatment as well. These findings demonstrate that, even a non-lethal concentration of GBS causes placental inflammation and oxidative stress, reduces trophoblast invasion of endothelial cells, and increases CXCL-8 and IL-6, key factors that participate in vascular dysregulation observed in several diseases. Furthermore, uvaol treatment prevented most of the GBS-provoked changes. Hence, uvaol could prevent the harmful effects of GBS infection for both the mother and the fetus.