Electrically Conductive Silicone-Based Nanocomposites Incorporated with Carbon Nanotubes and Silver Nanowires for Stretchable Electrodes.

Stretchable electrode materials have attracted great attention as next-generation electronic materials because of their ability to maintain intrinsic properties with rare damage when undergoing repetitive deformations, such as folding, twisting, and stretching. In this study, an electrically conductive PDMS nanocomposite was manufactured by combining the hybrid nanofillers of carbon nanotubes (CNTs) and silver nanowires (AgNWs). The amphiphilic isopropyl alcohol molecules temporarily adhered simultaneously to the hydrophobic CNT and hydrophilic AgNW surfaces, thereby improving the dispersity. As the CNT/AgNW ratio (wt %/wt %) decreased under the constant nanofiller content, the tensile modulus decreased and the elongation at break increased owing to the poor interaction between the AgNWs and matrix. The shear storage moduli of all nanocomposites were higher than the loss moduli, indicating the elastic behavior with a cross-linked network. The electrical conductivities of the nanocomposite containing the hybrid nanofillers were superior to those of the nanocomposite containing either CNT or AgNW at the same filler content (4 wt %). The hybrid nanofillers were rearranged and deformed by 5000 cyclic strain tests, relaxing the PDMS matrix chain and weakening the interfacial bonding. However, the elastic behavior was maintained. The dynamic electrical conductivities gradually increased under the cyclic strain tests due to the rearrangement and tunneling effect of the nanofillers. The highest dynamic electrical conductivity (10 S/m) was obtained for the nanocomposite consisting of 2 wt % of CNTs and 2 wt % of AgNWs.

Tat-DJ-1 protects neurons from ischemic damage in the ventral horn of rabbit spinal cord via increasing antioxidant levels.

The DJ-1 gene is highly conserved in diverse species and DJ-1 is known as an anti-oxidative stress factor. In this study, we investigated the neuroprotective effects of DJ-1 against ischemic damage in the rabbit spinal cord. Tat-DJ-1 fusion proteins were constructed to facilitate the penetration of DJ-1 protein into the neurons. Tat-1-DJ-1 fusion protein was administered to the rabbit 30 min after ischemia/reperfusion, and transient spinal cord ischemia was induced by occlusion of the aorta at the subrenal region for 15 min. The administration of Tat-DJ-1 significantly improved the Tarlov score compared to that in the Tat (vehicle)-treated group at 24, 48 and 72 h after ischemia/reperfusion. At 72 h after ischemia/reperfusion, the number of cresyl violet-positive neurons was significantly increased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. Lipid peroxidation as judged from the malondialdehyde levels was significantly decreased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. In contrast, superoxide dismutase and catalase levels were significantly increased in the Tat-DJ-1-treated group compared to that in the vehicle-treated group. This result suggests that DJ-1 protects neurons from ischemic damage in the ventral horn of the spinal cord via its antioxidant effects.

Repeated administration of PEP-1-Cu,Zn-superoxide dismutase and PEP-1-peroxiredoxin-2 to senescent mice induced by D-galactose improves the hippocampal functions.

Oxidative stress initiates age-related reduction in hippocampal neurogenesis and the use of antioxidants has been proposed as an effective strategy to prevent or attenuate the reduction of neurogenesis in the hippocampus. In the present study, we investigated the effects of Cu,Zn-superoxide dismutase (SOD1) and/or peroxiredoxin-2 (PRX2) on cell proliferation and neuroblast differentiation in the dentate gyrus in a model of D-galactose-induced aging model. For this study, we constructed an expression vector, PEP-1, fused PEP-1 with SOD1 or PRX2, and generated PEP-1-SOD1 and PEP-1-PRX2 fusion protein. The aging model was induced by subcutaneous injection of D-galactose (100 mg/kg) to 6-week-old male mice for 10 weeks. PEP-1, PEP-1-SOD1 and/or PEP-1-PRX2 fusion protein was intraperitoneally administered to these mice at 13-week-old once a day for 3 weeks and sacrificed at 30 min after the last administrations. The administration of PEP-1-SOD1 and/or PEP-1-PRX2 significantly improved D-galactose-induced deficits on the escape latency, swimming speeds, platform crossings, spatial preference for the target quadrant in Morris water maze test. In addition, the administration of PEP-1-SOD1 and/or PEP-1-PRX2 ameliorated D-galactose-induced reductions of cell proliferation and neuroblast differentiation in the dentate gyrus and significantly reduced D-galactose-induced lipid peroxidation in the hippocampus. These effects were more prominent in the PEP-1-SOD1-treated group with PEP-1-PRX2. These results suggest that a SOD1 and/or PRX2 supplement to aged mice could improve the memory deficits, cell proliferation and neuroblast differentiation in the dentate gyrus of D-galactose induced aged mice by reducing lipid peroxidation.

Effects of luteolin on spatial memory, cell proliferation, and neuroblast differentiation in the hippocampal dentate gyrus in a scopolamine-induced amnesia model.

OBJECTIVES: Luteolin, a common flavonoid from many plants, has various pharmacological activities, including a memory-improving effect. In this study, we investigated the effects of luteolin on spatial memory, cell proliferation, and neuroblast differentiation in the hippocampal dentate gyrus in a rat model of scopolamine (SCO)-induced amnesia. METHODS: Scopolamine was subcutaneously administered for 28 days via an Alzet minipump (44 mg/ml delivered at 2·5 µl/h) along with a daily intraperitoneal administration of vehicle (saline) 10 mg/kg luteolin or 5 mg/kg galantamine (GAL) (a control drug for acetylcholinesterase (AChE) inhibitor) for 28 days. RESULTS: The administration of SCO significantly decreased the spatial alteration percentage in the Y-maze test compared to that in the vehicle (saline)-treated group. The administration of luteolin or GAL significantly improved the spatial alteration percentage compared to that in the SCO-treated group. Similarly, the administration of SCO significantly decreased the cell proliferation (Ki67-positive cells) and neuroblast differentiation (doubleocortin-positive cells) in the dentate gyrus. The administration of luteolin or GAL significantly mitigated the SCO-induced reduction of Ki67- and doublecortin-immunoreactive cells in the dentate gyrus. In addition, the administration of luteolin significantly decreased the lipid peroxidation (malondialdehyde (MDA) levels) and increased the brain-derived neurotrophic factor (BDNF) and AChE levels in the hippocampal homogenates compared to the SCO-treated group. CONCLUSION: These results suggest that the luteolin treatment improves the SCO-induced reduction of cell proliferation and neuroblast differentiation in the dentate gyrus. The mechanism underlying the amelioration of SCO-induced amnesia by luteolin may be associated with the increase in BDNF, acetylcholine, and the decrease in lipid peroxidation.