Sellersharper5555

Previous studies have demonstrated that the sulfated polysaccharide named PRP-S16 could inhibit the proliferation, migration, and tube formation of endothelial cells in vitro. Here, its anti-angiogenic effect and mechanism in vivo were investigated by Lewis lung carcinoma (LLC) mice model. PRP-S16 significantly reduced the microvessel density (MVD) of tumor, exhibiting a high tumor growth inhibitory effect in LLC mice. All designed assays including quantitative real-time PCR, immunohistochemistry, enzyme-linked immunosorbent assay and western blotting showed that PRP-S16 reduced the mRNA and the protein expression of vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) in serum or tumor tissue of mice. Western blotting also detected decreased phosphorylated (p)-VEGFR-1, p-VEGFR-2, hypoxia-inducible factor-1α (HIF-1α), protein kinase B (Akt), and matrix metalloproteinases-9 (MMP-9). PRP-S16 had no adverse effects on angiogenesis in non-target organs. These findings suggested that the mechanism of anti-angiogenesis of PRP-S16 in vivo was due to inhibition of VEGF/VEGFR signaling pathway and it might be a promising candidate for tumor by anti-angiogenic therapy. V.As a natural fluorescent material, the fluorescent property and mechanism of lignin were elusive until now, which hindered the high value application of lignin fluorescence. Herein, we firstly probed the previous studies on lignin fluorescence and the results indicated that lignin microstructure was an important factor for its complex fluorescence property because of fluorophore interaction and aggregation behavior. Following the rules, lignin fluorescence was explored by analyzing its aggregation fluorescence behaviors and basic fluorescence properties based on the theory of traditional conjugated luminescence and aggregation-induced emission. It was demonstrated that intermicellar aggregation of loose lignin micelle made no substantial effect on lignin fluorescence, while intramicellar aggregation could induce the enhancement of lignin fluorescence before the micellar compactness exceeded a critical value. Combined with the physicochemical structures and fluorescence properties of lignin, aggregation-induced conjugation from phenylpropane units was believed as the main sources of the visible emission of lignin and different phenylpropane aggregates consequently formed the multi-fluorophore system in lignin micelle. Furthermore, lignin aggregation fluorescence behavior has great potential in its microstructure analysis and a case study of pH/ionic strength-induced solution behavior analysis was presented. This work provided a totally new prospective for lignin fluorescence. V.In this study, the effect of chondroitin sulphate nano-selenium (CS@Se) on Alzheimer's disease (AD) in mice was investigated. CS@Se alleviated anxiety and improved the spatial learning and memory impairment in AD mice. CS@Se significantly reduced cell oedema and pyknosis, protected the mitochondria, and improved abnormal changes in the ultrastructure of hippocampal neuron synapses of AD mice. Moreover, CS@Se significantly increased the levels of superoxide dismutase(SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase assay (Na+/K+-ATPase) and acetyltransferase (ChAT), and decreased the levels of malondialdehyde (MDA) and acetylcholinesterase (ChAE) in AD mice. Western blot results showed that CS@Se can attenuate excessive phosphorylation of tau (Ser396/Ser404) by regulating the expression of glycogen synthase kinase-3 beta (GSK-3β). In addition, CS@Se can activate the extracellular signal-regulated kinase 1/2 (ERK 1/2) and p38 mitogen-activated protein kinase (p38 MAPK) signalling pathways to inhibit nuclear transcription factor kappa B (NF-κB) nuclear translocation, thereby regulating the expression of pro-inflammatory cytokines. In summary, CS@Se can reduce oxidative stress damage, inhibit excessive tau phosphorylation, reduce inflammation to delay AD development, and increase the learning and memory capacities of AD mice. BI-2493 ic50 Changes in physicochemical and digestible characteristics of starches isolated from untreated and heat-moisture treated unpolished rice grains were investigated in this study. Heat-moisture treatment (HMT) at moisture content of 20%, 25% or 30% and heating temperature of 100 °C or 120 °C were applied for treating unpolished rice grains. The results indicated that granular morphology and crystalline structure of starches remained almost unchanged. However, a significant difference in the format and degree of agglomeration of starches of the rice grains treated at moisture content of 30% was observed. The HMT also suppressed the swelling and breakdown of the starch granules when treating at high moisture content and heating temperature. After HMT, amounts of resistant starch (RS) in the treated rice grains significantly increased as compared to that in the untreated rice grains. Moreover, the rice grains were heat-moisture treated with higher moisture contents or heating temperatures had higher RS contents. As a result, the rice grains treated at moisture content of 30% and heating temperature of 120 °C contained the highest amount of RS (49.1%), released the lowest blood glucose level and had GI value of 55, which is considered as low GI food. V.The material of CuS/polyvinyl alcohol-chitosan (CuS/PVACS) was prepared with a novel synthesis analysis. The crystallinity, morphological characteristics, and photocatalytic performance of the nano-materials were investigated by X-ray diffraction, field emission scanning electron microscopy X-ray photoelectron, and UV-vis spectrophotometry. The band gap values (Eg) was found as 2.50, and 2.04 eV for CuS, and CuS/PVACS nano-catalyst, respectively. The photo-degradation amount of the malachite green solutions which were degraded by CuS/PVACS in the UV-irradiation in 60 min was above 96.51%. The antibacterial properties of the CuS/PVACS has been evaluated versus (G+/G-) bacteria. The results of antibacterial performance indicated that CuS/PVACS nanocomposites have bacteriostatic behavior versus Escherichia coli, Pseudomonas syringae, Staphylococcus aureus and Streptococcus pneumoniae. V.