This study evaluated whether arginine (Arg) supplementation could attenuate gut injury induced by Escherichia coli lipopolysaccharide (LPS) challenge through an anti-inflammatory role in weaned pigs. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS þ 0·5 % Arg; (4) LPS þ 1·0 % Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h postinjection, pigs were killed for evaluation of small intestinal morphology and intestinal gene expression. Within 48 h of challenge, 0·5 % Arg alleviated the weight loss induced by LPS challenge (P¼ 0·025). In all three intestinal segments, 0·5 or 1·0 % Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P, 0·05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P,0·01). The 0·5 % Arg prevented the elevation of jejunal IL-6 mRNA abundance (P¼ 0·082), and jejunal (P¼0·030) and ileal (P¼ 0·039) TNF-a mRNA abundance induced by LPS challenge. The 1·0 % Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P¼ 0·053) and jejunal TNF-a mRNA abundance (P¼ 0·003) induced by LPS challenge. The 0·5 % Arg increased PPARg mRNA abundance in all three intestinal segments (P, 0·10), and 1·0 % Arg increased duodenal PPARg mRNA abundance (P¼ 0·094). These results indicate that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal proinflammatory cytokines through activating PPARg expression.
Nanoparticles are being increasingly recognized for their potential utility in biological applications including nanomedicine. The aim of this study is to investigate a new strategy to combine the ZnO nanoparticles with graphene for targeting photodynamic therapy (PDT) under visible light irradiation. Folic acid (FA), a targeting agent toward tumor cells, was conjugated onto graphene oxide (GO) via imide linkage. Using a simple and effective chemical precipitation method, a GO-FA-ZnO nanohybrid was then prepared. The combination of ZnO with GO-FA induced a remarkable improvement in tumor targeting, which has been demonstrated by the cellular uptake assay. Due to the high electrical conductivity of graphene, the interaction between graphene and ZnO, and the inhibition of aggregation, the hybrid of GO-FA and ZnO significantly enhances the photodynamic activity. It was noted that the photodynamic activity of the non-cytotoxic GO-FA-ZnO is mediated by reactive oxygen species (ROS) generation under visible light irradiation. Following the ROS generation, GO-FA-ZnO caused a significant decrease in cell viability, mitochondrial membrane potential, superoxide dismutase activity, catalase and glutathione peroxidase, as well as an increase in malonodialdehyde production.Moreover, GO-FA-ZnO induced apoptotic death by elevating the caspase-3 activity. The study presents a novel tumor targeting photosensitizer and a promising strategy in PDT for cancer treatment.
Sulfur amino acids (SAA), particularly methionine and cysteine, are critical for the gut to maintain its functions including the digestion, absorption and metabolism of nutrients, the immune surveillance of the intestinal epithelial layer and regulation of the mucosal response to foreign antigens. However, the metabolism of SAA in the gut, specifically the transmethylation of methionine, will result in a net release of homocysteine, which is shown to be associated with cardiovascular disease and stroke. Furthermore, the extensive catabolism of dietary methionine by the intestine or by luminal microbes may result in a decrease in nutritional efficiency. Therefore, the regulation of SAA metabolism in the gut is not only nutritionally relevant, but also relevant to the overall health and well-being. The superiority of DL-2-hydroxy-4-methylthiobutyrate to DL-methionine in decreasing homocysteine production, alleviating stress responses, and reducing the first-pass intestinal metabolism of dietary methionine may provide a promising implication for nutritional strategies to manipulate SAA metabolism and thus to improve the nutrition and health status of animals and perhaps humans.
Supplementation of branched-chain amino acids (BCAA) has been demonstrated to promote skeletal muscle mass gain, but the mechanisms underlying this observation are still unknown. Since the regulation of muscle mass depends on a dynamic equilibrium (fasted losses–fed gains) in protein turnover, the aim of this study was to investigate the effects of BCAA supplementation on muscle protein synthesis and degradation in fed/fasted states and the related mechanisms. Fourteen 26- (Experiment 1) and 28-day-old (Experiment 2) piglets were fed reduced-protein diets without or with supplemental BCAA. After a four-week acclimation period, skeletal muscle mass and components of anabolic and catabolic signaling in muscle samples after overnight fasting were determined in Experiment 1. Pigs in Experiment 2 were implanted with carotid arterial, jugular venous, femoral arterial and venous catheters, and fed once hourly along with the intravenous infusion of NaH13CO3 for 2 h, followed by a 6-h infusion of [1-13C]leucine. Muscle leucine kinetics were measured using arteriovenous difference technique. The mass of most muscles was increased by BCAA supplementation. During feeding, BCAA supplementation increased leucine uptake, protein synthesis, protein degradation and net transamination. The greater increase in protein synthesis than in protein degradation resulted in elevated protein deposition. Protein synthesis was strongly and positively correlated with the intramuscular net production of α-ketoisocaproate (KIC) and protein degradation. Moreover, BCAA supplementation enhanced the fasted-state phosphorylation of protein translation initiation factors and inhibited the protein-degradation signaling of ubiquitin-proteasome and autophagy-lysosome systems. In conclusion, supplementation of BCAA to reduced-protein diet increases fed-state protein synthesis and inhibits fasted-state protein degradation, both of which could contribute to the elevation of skeletal muscle mass in piglets. The effect of BCAA supplementation on muscle protein synthesis is associated with the increase in protein degradation and KIC production in the fed state.
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