Novel antiviral cotton fabrics impregnated with different formulations based on Chitosan (CH), citric acid (CA), and Copper (Cu) were developed. CA was selected as a CH crosslinker agent and Cu salts as enhancers of the polymer antimicrobial activity. The characterization of the polymeric-inorganic formulations was assessed by using atomic absorption spectroscopy, X-ray diffraction, Fourier transform infrared and UV-Vis spectroscopy, as well as thermogravimetric analysis. The achieved data revealed that CuO nanoparticles were formed by means of chitosan and citric acid in the reaction media. The antiviral activity of CH-based formulations against bovine alphaherpesvirus and bovine betacoronavirus was analyzed. Cotton fabrics were impregnated with the selected formulations and the antiviral properties of such textiles were examined before and after 5 to 10 washing cycles. Herpes simplex virus type 1 was selected to analyze the antiviral activities of the functionalized cotton fabrics. The resulting impregnated textiles exhibited integrated properties of good adhesion without substantially modifying their appearance and antiviral efficacy (~ 100%), which enabling to serve as a scalable biocidal layer in protective equipment's by providing contact killing against pathogens. Thus, the results revealed a viable contribution to the design of functional-active materials based on a natural polymer such as chitosan. This proposal may be considered as a potential tool to inhibit the propagation and dissemination of enveloped viruses, including SARS-CoV-2.
Age-related macular degeneration (AMD) is among the main pathologies leading to blindness in adults and has currently no cure or effective treatment. Selective apoptosis of retina pigment epithelial (RPE) cells results in the progressive loss of photoreceptor neurons, with the consequent gradual vision loss. Oxidative stress plays an important role in this process. We have previously determined that activation of RXRs protects rat photoreceptor neurons from oxidative stress-induced apoptosis. In this study we investigated whether RXR ligands prevented apoptosis in an RPE cell line, D407 cells, exposed to hydrogen peroxide (H2O2). H2O2 induced apoptosis of D407 cells, promoting p65NFκB nuclear translocation, increasing Bax mRNA expression, activating caspase-3 and altering cell morphology. We show, for the first time, that HX630, a RXR pan-agonist, protected D407 cells from H2O2-induced apoptosis, preventing p65NFκB nuclear translocation, increasing Bclxl and PPARγ mRNA levels and simultaneously decreasing Bax mRNA levels and caspase-3 activation. Pretreatment with a RXR antagonist blocked HX630 protection. LG100754, which binds RXRs but only activates heterodimers and is an antagonist of RXR homodimers, also had a protective effect. In addition, only agonists known to bind to RXR/PPARγ were protective. As a whole, our results suggest that RXR activation protects RPE cells from oxidative stress-induced apoptosis and this protection might involve signaling through a heterodimeric receptor, such as RXR/PPARγ. These data also imply that RXR agonists might provide potential pharmacological tools for treating retina degenerative diseases.
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