Characteristics, antimicrobial capacity, and antioxidant potential of electrospun zein/polyvinyl alcohol nanofibers containing thymoquinone and electrosprayed resveratrol nanoparticles.

The aim of the present study was to fabricate, characterize, and evaluate the in vitro antimicrobial and antioxidant properties of zein/polyvinyl alcohol (ZN/PVA) nanofibers containing 2% and 4% of thymoquinone (TQ), either alone or in combination with electrosprayed ZN nanoparticles containing 1% and 2% of resveratrol (RS). According to scanning electron microscopy analysis, the diameter of nanofibers and nanoparticles increased with increasing TQ and RS concentrations, respectively. The molecular interaction between ZN or PVA polymers and TQ or RS was confirmed by Fourier transform infrared spectroscopy. Thermogravimetric analysis showed that the thermal stability of nanofibers did not change with the addition of TQ and RS. Moreover, incorporation of TQ in nanofibers along with RS nanoparticles increased their antibacterial and free radical scavenging activities based on broth dilution and DPPH methods, respectively (p ≤ .05). Escherichia coli O157:H7 (as a Gram-negative pathogenic bacteria) was more resistant to all treatments than Staphylococcus aureus (as a Gram-positive pathogenic bacteria). In addition, the combined use of TQ in nanofibers and RS nanoparticles had antagonistic antibacterial and synergistic antioxidant effects. The best results were obtained with ZN/PVA nanofiber containing 4% TQ and electrosprayed with 2% RS nanoparticles (p ≤ .05). According to the results of the present study, biodegradable ZN/PVA nanofiber containing TQ and electrosprayed with RS nanoparticles can be used as a novel active packaging material in the food industry.

Aerobic endurance training improves nonalcoholic fatty liver disease (NAFLD) features via miR-33 dependent autophagy induction in high fat diet fed mice.

Due to changes in life style, obesity and obesity related complication such as insulin resistance, type 2 diabetes and non-alcoholic fatty liver disease caused worldwide health problems. Regular exercise has been frequently prescribed to combat metabolic complication of obesity but its molecular mechanism has not been fully illustrated. We investigated molecular mechanism of lipid lowering effect of exercise training in high fat diet fed mice by focusing on miR-33 expression and autophagy pathway. 24 mice were assigned to normal chow (NC) (n=8), high-fat diet (HFD) (n=16) group and subjected to NC and HFD for 13-weeks. HFD groups were divided to sedentary (HFD n=8) or continuous endurance training (HFD+CET, n=8) subgroups. The HFD+CET mice were subjected to treadmill running for 10-weeks in 23-week HFD course. HFD increased body weight, fasting blood sugar, triglyceride, cholesterol, aspartate aminotransferase (AST), alanine aminotransferase (ALT), liver lipogenic genes expression and reduced miR-33 mRNA expression and autopahgy pathway while training program reversed them. Exogenous miR-33 mimic sequence induced autophagy and reduced lipogenesis in HepG2 cells. Autophagy induction by rapamycin reduced lipogenesis and autophagy inhibition by chloroquine, enhanced lipogenesis in HepG2 cells. These findings suggest that aerobic exercise training as a non-pharmacological therapy exerts its lipid lowering effects by miR-33 dependent autophagy induction.

Palmitate induces SHIP2 expression via the ceramide-mediated activation of NF-κB, and JNK in skeletal muscle cells.

AIMS: Elevated plasma free fatty acids impair the insulin signaling by induction of the expression of protein phosphatases. However, the effect of palmitate on SH2-containing inositol 5'-phosphatase 2 (SHIP2) expression has not been investigated. Here we investigated the effects of palmitate on SHIP2 expression and elucidated the underlying mechanisms in skeletal muscle cells. MAIN METHODS: SHIP2 mRNA and protein levels were measured in C2C12 myotubes exposed to palmitate. Specific inhibitors were used to identify the signaling pathways involved in SHIP2 expression. KEY FINDINGS: The results showed that 0.5mM palmitate significantly upregulates the mRNA and protein levels of SHIP2 in C2C12 cells. To address the role of palmitate intracellular metabolites in SHIP2 expression, the myotubes were treated with palmitate in the presence of ceramide and diacylglycerol synthesis inhibitors. The results demonstrated that only ceramide synthesis inhibition could prevent palmitate-induced SHIP2 expression in these cells. In addition, the incubation of muscle cells with different concentrations of C2-ceramide dose-dependently enhanced SHIP2 expression. Furthermore, the inhibition of both JNK and NF-κB pathways could prevent ceramide-induced SHIP2 expression in myotubes. SIGNIFICANCE: These findings suggest that palmitate contributes to SHIP2 overexpression in skeletal muscle via the mechanisms involving the activation of ceramide-JNK and NF-κB pathways.