Asymmetric supercapacitors based on SnNiCoS ternary metal sulfide electrodes.

While metal sulfides have extensively investigated as electrode materials for supercapacitors, the further optimization of their material system is still necessary to achieve satisfied performance. In this work, we reported the synthesis of ternary metal sulfide SnNiCoS and its application as electrode material of asymmetric supercapacitors, in which active carbon is used as the other electrode. For control experiments, asymmetric supercapacitors based on single metal sulfide CoS and binary metal sulfide NiCoS are also fabricated and investigated. The results show that the nanospherical SnNiCoS achieves the best performance. Ternary sulphide materials offer more redox than corresponding single-metal sulphides due to the synergy among various transition metal elements. The specific capacitance is 18.6 F cm-2at current density of 5 mA·cm-2. An energy density of 937.2µWh cm-2is achieved at a power density of 4000µW·cm-2. After 8000 cycles, the capacity retention rate is 82.9%. Present work indicates that SnNiCoS ternary metal sulfide could be a promising composite for high performance supercapacitors.

Casticin alleviates lipopolysaccharide-induced inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells through Nrf2/Keap1 and NF-κB pathways.

Asthma is one of the most common chronic inflammatory diseases of childhood, characterized by airway inflammation, mucus hypersecretion, and accumulation of extracellular matrix proteins. Casticin is an active compound that possesses broad biological activities including anti-inflammatory effect. However, the effect of casticin on asthma remains unknown. The aim of the present study was to evaluate the effect and mechanism of casticin on inflammatory responses and expression of mucus and extracellular matrix in human airway epithelial cells. The results showed that lipopolysaccharide induced the mRNA and protein levels of IL-6, IL-8, MUC5AC, collagen type I, and fibronectin in 16-HBE cells, whereas casticin treatment significantly inhibited the induction of lipopolysaccharide. Casticin induced Nrf2/Keap1 and inhibited nuclear factor κB pathways in 16-HBE cells. Knockdown of Nrf2 attenuated the effect of casticin on production of IL-6 and IL-8, expression of MUC5AC, collagen type I, and fibronectin in 16-HBE cells. In conclusion, the results indicated that casticin might be a novel therapeutic strategy for the treatment of asthma.