RESUMO
Developing cost-effective, efficient, and durable catalysts for oxygen evolution reactions (OER) is the key for promoting large-scale H2 production through electrochemical water splitting. Herein, we report a facile method for fabricating an NiFe@NiCr-LDH catalyst toward alkaline OER. The electronic microscopy technique revealed that it has a well-defined heterostructure at the interface between the NiFe and NiCr phases. In 1.0 M KOH, the as-prepared NiFe@NiCr-LDH catalyst shows excellent catalytic performance, evidenced by an overpotential of 266 mV at the current density of 10 mA cm-2 and a small Tafel slope of 63 mV dec-1; both are comparable with the RuO2 benchmark catalyst. It also exhibits robust durability in long-term operation, manifested by a 10% current decay in 20 h, which is superior to that of the RuO2 catalyst. Such excellent performance is attributed to the interfacial electron transfer that occurs at the interfaces of the heterostructure, and the Fe(III) species facilitate the formation of Ni(III) species as active sites in NiFe@NiCr-LDH. This study offers a feasible strategy for preparing a transition metal-based LDH catalyst for OER toward H2 production and other electrochemical energy technologies.
RESUMO
Intracerebral hemorrhage (ICH) is a common neurological condition that causes severe disability and even death. Even though the mechanism is not clear, increasing evidence shows the efficacy of atorvastatin on treating ICH. In this study, we examined the impact of atorvastatin on the NOD-like receptor protein 3 (NLRP3) inflammasome and inflammatory pathways following ICH. Mouse models of ICH were established by collagenase injection in adult C57BL/6 mice. IHC mice received atorvastatin treatment 2 h after hematoma establishment. First, the changes of glial cells and neurons in the brains of ICH patients and mice were detected by immunohistochemistry and western blotting. Second, the molecular mechanisms underlying the microglial activation and neuronal loss were evaluated after the application of atorvastatin. Finally, the behavioral deficits of ICH mice without or with the treatment of atorvastatin were determined by neurological defect scores. The results demonstrated that atorvastatin significantly deactivated glial cells by reducing the expression of glial fibrillary acidic protein (GFAP), Ionized calcium binding adapter molecule 1 (Iba1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in ICH model mice. For inflammasomes, atorvastatin also showed its efficacy by decreasing the expression of NLRP3, cleaved caspase-1, and IL-1ß in ICH mice. Moreover, atorvastatin markedly inhibited the upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), which indicated deactivation of NLRP3 inflammasomes. By inhibiting the activities of inflammasomes in glial cells, neuronal loss was partially prevented by suppressing the apoptosis in the brains of ICH mice, protecting them from neurological defects.
