Extraction of Glyoxylic Acid Stabilized Lignin from Lignocellulosic Biomass for a Natural Sunscreen Additive

Natural lignin has been considered a promising additive for ultraviolet (UV) protection cosmetics applications. Nevertheless, its potential application in cosmetics production is impeded by its inherent dark coloration due to structural damage incurred during the industrial lignin extraction process. In this study, glyoxylic acid (GA) was used to prevent lignin condensation during lignin extraction using an acid recycled hydrotrope (p-toluenesulfonic acid, p-TsOH). Further processing of the GA stabilized lignin yielded lignin nanospheres (LNPs) for a natural sunscreen additive. Incorporating 3% and 4% LNPs into a baseline SPF10 commercial sunscreen resulted in lignin-based sunscreen with SPF values of 37.2 ± 2.55 and 58.74 ± 2.14, respectively. These exceeded the SPF levels observed in commercial sunscreens with SPF30 and SPF50. Furthermore, the pretreated cellulose residue was utilized in the production of pulp fibers for papermaking. It was observed that the ring crush strength index of the paper, achieved by incorporating 15 wt % fibers into softwood pulp, reached a notable value of 2.98 ± 0.10 N·m/g. The tear index and tensile index of the produced paper, augmented with a 5 wt % addition of fibers, were as high as 4.77 ± 0.41 mN·m2/g and 9.49 ± 0.27 N·m/g, respectively. Therefore, a new strategy for stabilized lignin extraction and lignocellulose biomass valorization was proposed in this study

Melatonin Maintains Homeostasis and Potentiates the Anti-inflammatory Response in Staphylococcus aureus-Induced Mastitis through microRNA-16b/YAP1

Staphylococcus aureus is a highly infectious pathogen and is a considerable threat to food hygiene and safety. Although melatonin is thought to exert an ameliorative effect on bovine mastitis, the regulatory mechanisms are unclear. In this study, we first verified the therapeutic effect of melatonin against S. aureus in vitro and in vivo, a screening of differentially expressed miRNAs and mRNAs among the blank, and S. aureus and melatonin + S. aureus groups by high-throughput sequencing identified miR-16b and YAP1, which exhibited 1.95-fold upregulated and 1.05-fold downregulated expression, respectively. Moreover, epigenetic studies showed that S. aureus inhibited miR-16b expression by methylation (increased DNMT1 expression). Additionally, the DNMT1 expression level was significantly decreased by melatonin treatment, which might indicate that the inhibition of DNMT1 by melatonin reduces the effect of S. aureus on miR-16b. The flow cytometry, scanning and transmission electron microscopy, EdU assay, and cell morphology results indicated that miR-16b in bovine mammary epithelial cells (in vitro) and in mice (in vivo) can modulate the maintenance of homeostasis and potentiate the anti-inflammatory response. In addition, YAP1 was demonstrated to be the target gene of miR-16b through quantitative real-time polymerase chain reaction, western blot, RNA immunoprecipitation, and functional assays. This study indicates that melatonin inhibits S. aureus-induced inflammation via microRNA-16b/YAP1-mediated regulation, and these findings might provide a new strategy for the prevention of bovine mastitis, facilitating further studies good of zoonotic diseases caused by S. aureus infection

Melatonin Maintains Homeostasis and Potentiates the Anti-inflammatory Response in Staphylococcus aureus-Induced Mastitis through microRNA-16b/YAP1

Staphylococcus aureus is a highly infectious pathogen and is a considerable threat to food hygiene and safety. Although melatonin is thought to exert an ameliorative effect on bovine mastitis, the regulatory mechanisms are unclear. In this study, we first verified the therapeutic effect of melatonin against S. aureus in vitro and in vivo, a screening of differentially expressed miRNAs and mRNAs among the blank, and S. aureus and melatonin + S. aureus groups by high-throughput sequencing identified miR-16b and YAP1, which exhibited 1.95-fold upregulated and 1.05-fold downregulated expression, respectively. Moreover, epigenetic studies showed that S. aureus inhibited miR-16b expression by methylation (increased DNMT1 expression). Additionally, the DNMT1 expression level was significantly decreased by melatonin treatment, which might indicate that the inhibition of DNMT1 by melatonin reduces the effect of S. aureus on miR-16b. The flow cytometry, scanning and transmission electron microscopy, EdU assay, and cell morphology results indicated that miR-16b in bovine mammary epithelial cells (in vitro) and in mice (in vivo) can modulate the maintenance of homeostasis and potentiate the anti-inflammatory response. In addition, YAP1 was demonstrated to be the target gene of miR-16b through quantitative real-time polymerase chain reaction, western blot, RNA immunoprecipitation, and functional assays. This study indicates that melatonin inhibits S. aureus-induced inflammation via microRNA-16b/YAP1-mediated regulation, and these findings might provide a new strategy for the prevention of bovine mastitis, facilitating further studies good of zoonotic diseases caused by S. aureus infection