BackgroundPropolis, a polyphenol-rich natural product, has been used as a functional food in anti-inflammation. However, its bioactive components and mechanisms have not been fully elucidated.To discover the bioactive components and anti-inflammatory mechanism, we prepared and separated 8 subfractions from ethyl acetate extract of Chinese propolis (EACP) and investigated the mechanism in oxidized low density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage.MethodsEight subfractions were prepared and separated from ethyl acetate extract of Chinese propolis (EACP) with different concentrations of methanol-water solution, and analysed its chemical constituents by HPLC-DAD/Q-TOF-MS. Then 80% confluent HUVECs were stimulated with 40 μg/mL ox-LDL. Cell viability and apoptosis were evaluated by Sulforhodamine B (SRB) assay and Hoechst 33,258 staining, respectively. Levels of caspase 3, PARP, LC3B, p62, p-mTOR, p-p70S6K, p-PI3K, p-Akt, LOX-1 and p-p38 MAPK were assessed by western blotting and immunofluorescence assay, respectively. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were measured with fluorescent probes.ResultsEach subfraction exhibited similar protective effect although the contents of chemical constituents were different. EACP attenuated ox-LDL induced HUVECs apoptosis, depressed the ratio of LC3-II/LC3-I and enhanced the p62 level. In addition, treatment with EACP also activated the phosphorylation of PI3K/Akt/mTOR, and deactivated the level of LOX-1 and phosphorylation of p38 MAPK. The overproduction of ROS and the damage of MMP were also ameliorated after ECAP treatment.ConclusionsThese findings indicated that the bioactive component of propolis on anti-inflammatory activity was not determined by a single constituent, but a complex interaction including flavonoids, esters and phenolic acids. EACP attenuated ox-LDL induced HUVECs injury by inhibiting LOX-1 level and depressed ROS production against oxidative stress in ox-LDL induced HUVECs, further to activate PI3K/Akt/mTOR pathway and deactivate p38 MAPK to inhibit apoptosis and autophagy, which provide novel insights into the potential application of propolis on modulating chronic inflammation.
A cellular material in the form of 3-layered sandwich structure material was prepared via sole use of mechanical stirring without any use of a foaming agent, while Tween-80 was employed as a foam stabilizer via a developed in-situ mold casting. The resulting structure displayed a good appearance with no visual defects. The 3-layered composition of the sandwish structure, "nonporous resin layer-porous foam layer-nonporous resin layer", was examined in terms of the microstructure, density & density distribution, pulverization ratio, mechanical strength, insulation and flame retardant performance. It was indicated from the results that the bonding between the resin layer and foam layer was tight, while the tensile rupture always occurred in the porous layer. Also, the density of the sandwich structure material was symmetrical with "saddle" distribution, and a uniform density for any given layer. The increase in the density at the interface layer provided a good interpretation for the tensile rupture never occurred at the interface. The brittleness resistance of the developed material was significantly improved, and the pulverization ratio was sharply decreased from 9.93% to 0.31%. The material acquired a thermal conductivity and limiting oxygen index (LOI) of 0.0241 W/m ⋅ K and 29.92%, respectively, indicating potential use of such materials broadly in fields of insulation and flame retardancy.
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