Carbon-Coated ZnS-FeS2 Heterostructure as an Anode Material for Lithium-Ion Battery Applications.

The construction of carbon-coated heterostructures of bimetallic sulfide is an effective technique to improve the electrochemical activity of anode materials in lithium-ion batteries. In this work, the carbon-coated heterostructured ZnS-FeS2 is prepared by a two-step hydrothermal method. The crystallinity and nature of carbon-coating are confirmed by the investigation of XRD and Raman spectroscopy techniques. The nanoparticle morphology of ZnS and plate-like morphology of FeS2 is established by TEM images. The chemical composition of heterostructure ZnS-FeS2@C is discovered by an XPS study. The CV results have disclosed the charge storage mechanism, which depends on the capacitive and diffusion process. The BET surface area (37.95 m2g-1) and lower Rct value (137 Ω) of ZnS-FeS2@C are beneficial to attain higher lithium-ion storage performance. It delivered a discharge capacity of 821 mAh g-1 in the 500th continuous cycle @ A g-1, with a coulombic efficiency of around 100%, which is higher than the ZnS-FeS2 heterostructure (512 mAh g-1). The proposed strategy can improve the electrochemical performance and stability of lithium-ion batteries, and can be helpful in finding highly effective anode materials for energy storage devices.

Morin, a dietary flavonoid, exhibits anti-fibrotic effect and induces apoptosis of activated hepatic stellate cells by suppressing canonical NF-κB signaling.

In experimental liver fibrosis, activated hepatic stellate cells (HSCs) play a central role and thus, induction of apoptosis of activated HSCs is a promising therapeutic strategy for liver fibrosis. The present study was designed to elucidate the molecular mechanisms of the pro-apoptotic effects of morin, a dietary flavonoid, in vitro and in vivo. Culture-activated human HSCs (LX-2 cells) were treated with morin (50 µM) for 24 and 48 h, and the mechanism of cell death induced by morin was evaluated. Also, the anti-fibrotic and pro-apoptotic effect of morin in diethylnitrosamine (DEN)-induced fibrotic rats were determined. Morin induced apoptosis in cultured LX-2 cells by preventing the nuclear translocation of nuclear factor-κBp65 (NF-κBp65) by inhibiting NF-κB activation via inhibition of IκBα degradation and thereby suppressing anti-apoptotic proteins and activating caspases. In fibrotic rats, morin treatment resulted in inhibition of canonical NF-κB signaling and induction of apoptosis, mainly by downregulating Bcl-2, upregulating Bax and cyt c and by activation of caspase-9 and caspase-3. Translocation of phosphatidylserine to the outer membrane, altered nuclear morphology and DNA fragmentation confirmed the induction of apoptosis by morin. Overall, morin treatment ameliorated experimental liver fibrosis, most likely through induction of apoptosis by inhibiting canonical NF-κB signaling in activated HSCs. It is therefore postulated that morin is a potential therapeutic candidate for liver fibrosis.

Morin ameliorates chemically induced liver fibrosis in vivo and inhibits stellate cell proliferation in vitro by suppressing Wnt/ß-catenin signaling.

The anti-fibrotic effect of morin was examined in LX-2 cells (culture-activated human hepatic stellate cells) and in diethylnitrosamine induced rat model of liver fibrosis. The in vitro study was designed to determine whether morin affects the survival of cultured LX-2 cells, while the in vivo study was designed to evaluate the antioxidant and anti-fibrotic efficacy of morin on diethylnitrosamine induced liver fibrosis in male albino Wistar rat. The activities of liver function enzymes in serum, liver lipid peroxide levels, activities of serum antioxidant enzymes and liver architecture were monitored to cast light on the antioxidant and hepatoprotective nature of morin. To establish the anti-fibrotic effects of morin, the levels of key Wnt signaling molecules which are strongly associated with the signal transduction pathway of HSC activation were measured. Overall, from the in vitro results, it was observed that morin at 50 µM concentration inhibited the proliferation of cultured LX-2 cells, inhibited Wnt signaling and induced G1 cell cycle arrest. The in vivo results further confirmed that morin by downregulating the expressions of GSK-3ß, ß-catenin and cyclin D1 ameliorated DEN-induced liver fibrosis. Hence morin could be employed as a promising chemopreventive natural supplement for liver fibrosis.