This study compared the loading ability of various carotenoids into liposomal membrane, lipid peroxidation inhibition capacity, storage stability and in vitro release behavior in simulated gastrointestinal (GI) media. It was found that carotenoids exhibited various incorporating abilities into liposomes ranging from the strongest to the weakest: lutein > β-carotene > lycopene > canthaxanthin. A similar trend was also observed in their antioxidant activities against lipid peroxidation during preparation. Storage measurements demonstrated that a liposomal membrane can strongly retain β-carotene and lutein, whereas this effect was not pronounced for lycopene and canthaxanthin. In vitro release experiments showed that lutein and β-carotene were hardly released in a simulated gastric fluid, while displaying a slow and sustained release in a simulated intestinal fluid. By contrast, lycopene and canthaxanthin underwent fast and considerable release in GI media. Dynamic light scattering indicated that carotenoid incorporation strongly affected the particle stability and dispersion during preparation and GI incubation. The differences in molecular release may be attributed to the different modulating effects of carotenoids. Our results may guide the potential application of liposomes as carriers for the controlled delivery of carotenoids in nutraceutical and functional foods.

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Tumor necrosis factor receptor-associated factor 5 (TRAF5) is an adaptor protein of the tumor necrosis factor (TNF) receptor superfamily and the interleukin-1 receptor/Toll-like receptor superfamily and plays important roles in regulating multiple signaling pathways. This study was conducted to investigate the role of TRAF5 in the context of brain ischemia/reperfusion (I/R) injury. Transient occlusion of the middle cerebral artery was performed on TRAF5 knockout mice (KO), neuron-specific TRAF5 transgene (TG), and the appropriate controls. Compared with the WT mice, the TRAF5 KO mice showed lower infarct volumes and better outcomes in the neurological tests. A low neuronal apoptosis level, an attenuated blood-brain barrier (BBB) disruption and an inhibited inflammatory response were exhibited in TRAF5 KO mice. TRAF5 TG mice exhibited an opposite phenotype. Moreover, the Akt/FoxO1 signaling pathway was enhanced in the ischemic brains of the TRAF5 KO mice. These results provide the first demonstration that TRAF5 is a critical mediator of I/R injury in an experimental stroke model. The Akt /FoxO1 signaling pathway probably plays an important role in the biological function of TRAF5 in this model.

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Study on alternative methods to hydrodesulfurization is always an interesting area, because of the ineffectiveness for hydrodesulfurization to remove some cyclic sulfur compounds (S-compounds) and the high cost from harsh operation conditions and expensive catalyst, among which oxidative desulfurization (ODS) using ionic liquids (ILs) as solvent is intensively studied recently. Here, we synthesize a series of Brønsted–Lewis acidic ILs of N-methylpyrrolidonium zinc chloride ([Hnmp]­Cl x /(ZnCl2) y , x:y from 2:1 to 1:2) and investigate the ODS of both model diesel fuel composed of n-octane and dibenzothiophene and real FCC feedstock where such ILs are used as extractant and catalyst and 30 wt % H2O2 is used as oxidant, involving the factors such as IL composition (or x:y), temperature, dose of oxidant (or molar ratio of O/S), dose of IL (or mass ratio of IL/oil), recycling of IL and multistage desulfurization. IL composition has an important effect on sulfur removal (S-removal) efficiency, and [Hnmp]­Cl/ZnCl2 (x:y = 1, the structure nature was characterized with ESI-MS and FT-IR) shows the highest desulfurization capability with good recyclability. With [Hnmp]­Cl/ZnCl2, the S-content in model diesel fuel can be reduced to <1 ppm from 500 ppm with 99.9% S-removal at 75 °C, IL/oil = 1/3 and O/S = 8 after only one stage, while the sulfur removal for real FCC diesel fuel is less than 38% in one stage and can reach 83% after five stages, which might be ascribed to more-complex S-species in real fluidized catalytic cracking (FCC) diesel fuel as indicated by gas chromatography–sulfur chemiluminescence detection (GC-SCD) chromatogram analyses. The sulfur content (S-content) in FCC diesel fuel, however, can be reduced to 5.3 ppm with a total S-removal of 97.6% after five-stage ODS with one more extractive desulfurization with furfural as the extractant. This work shows that such Brønsted–Lewis acidic ILs are potential solvents used in ODS to produce clean fuel oils.

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Stroke is the second leading cause of mortality and the most common cause of long-term disability worldwide (Mathers et al. 2009). Over 15 million people suffer from stroke each year, and approximately 80-85% of these cases are ischemic stroke. Accumulating evidence from the past two decades has suggested that the oxidative stress associated with the excessive production of reactive oxygen species (ROS) has a profound effect on ischemic stroke pathogenesis (El Kossi Abbreviations used: HO-1, heme oxygenase 1; Nrf2, nuclear factor-E2-related factor 2; ROS, reactive oxygen speciesSHPS-1 MT, SHPS-1 mutant; tMCAO, transient middle cerebral artery occlusion. , , Abstract Src homology 2 domain-containing protein tyrosine phosphatase substrate-1 (SHPS-1), also known as Signal-regulatory protein alpha (SIRPa) or SIRPA is a transmembrane protein that is predominantly expressed in neurons, dendritic cells, and macrophages. This study was conducted to investigate the role of SHPS-1 in the oxidative stress and brain damage induced by acute focal cerebral ischemia. Wildtype (WT) and SHPS-1 mutant (MT) mice were subjected to middle cerebral artery occlusion (60 min) followed by reperfusion. SHPS-1 MT mice had significantly reduced infarct volumes and improved neurological function after brain ischemia. In addition, neural injury and oxidative stress were inhibited in SHPS-1 MT mice. The mRNA and protein levels of the antioxidant genes nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase 1 were up-regulated in SHPS-1 MT mice. The SHPS-1 mutation suppressed the phosphorylation of SHP-1 and SHP-2 and increased the phosphorylation of Akt and GSK3b. These results provide the first demonstration that SHPS-1 plays an important role in the oxidative stress and brain injury induced by acute cerebral ischemia. The activation of Akt signaling and the up-regulation of Nrf2 and heme oxygenase 1 likely account for the protective effects that were observed in the SHPS-1 MT mice.