Fe3O4-doped mesoporous carbon cathode with a plumber's nightmare structure for high-performance Li-S batteries.

Shuttling of lithium polysulfides and slow redox kinetics seriously limit the rate and cycling performance of lithium-sulfur batteries. In this study, Fe3O4-dopped carbon cubosomes with a plumber's nightmare structure (SP-Fe3O4-C) are prepared as sulfur hosts to construct cathodes with high rate capability and long cycling life for Li-S batteries. Their three-dimensional continuous mesochannels and carbon frameworks, along with the uniformly distributed Fe3O4 particles, enable smooth mass/electron transport, strong polysulfides capture capability, and fast catalytic conversion of the sulfur species. Impressively, the SP-Fe3O4-C cathode exhibits top-level comprehensive performance, with high specific capacity (1303.4 mAh g-1 at 0.2 C), high rate capability (691.8 mAh gFe3O41 at 5 C), and long cycling life (over 1200 cycles). This study demonstrates a unique structure for high-performance Li-S batteries and opens a distinctive avenue for developing multifunctional electrode materials for next-generation energy storage devices.

Geniposide attenuates cadmium­induced oxidative stress injury via Nrf2 signaling in osteoblasts.

Geniposide, as a type of iridoid glycoside, has antioxidative capacity. However, the mechanism underlying the effect of geniposide in cadmium (Cd)­induced osteoblast injury remains only partly elucidated. In the present study, Cell Counting Kit­8 (CCK­8) was used to determine MC­3T3­E1 cell viability. Flow cytometry was used to determine the rate of apoptosis and levels of reactive oxygen species (ROS). Oxidative stress­related factors were assessed using enzyme­linked immunosorbent method (ELISA). Quantitative real­time polymerase chain reaction (qPCR) and western blotting were used to evaluate apoptosis­ and bone formation­related genes and nuclear factor erythroid 2­related factor (Nrf2) signaling. It was demonstrated that geniposide increased the viability of the Cd­treated MC­3T3­E1 cells. Geniposide decreased apoptosis and ROS accumulation compared to these parameters in the Cd group. Geniposide attenuated oxidative stress­related factors, malondialdehyde and lactate dehydrogenase and increased antioxidant key enzyme superoxidase dismutase (SOD). The expression levels of Bax, Bcl­2 and survivin were modulated by geniposide. Additionally, the mRNA and protein expression of the receptor activator of NF­κB ligand (RANKL) and osterix were significantly increased, while osteoprotegerin was decreased by geniposide treatment compared to the Cd groups. Geniposide also enhanced Nrf2, heme oxygenase­1 (HO­1) and NAD(P)H quinone dehydrogenase 1 (NQO1) expression. The present study identified a potential agent for the treatment of Cd­induced osteoblast injury.