Dihydroquercetin improves experimental acute liver failure by targeting ferroptosis and mitochondria-mediated apoptosis through the SIRT1/p53 axis.

Background: Ferroptosis and mitochondria-mediated apoptosis are both involved in the pathogenesis of acute liver failure (ALF). Ferroptosis-produced reactive oxygen species (ROS) trigger the chain oxidation of polyunsaturated phospholipids and promote mitochondrial apoptosis. Dihydroquercetin (DHQ) also plays an important protective role against liver injury.

Rapid Formation of Epitaxial Oxygen Evolution Reaction Catalysts on Dendrites with High Catalytic Activity and Stability.

Oxygen evolution reaction is an essential but kinetically sluggish step in many energy storage and conversion processes and therefore is in pursuit of highly efficient and stable catalysts. Although nanosized transition-metal-based oxides/hydroxides exhibit high catalytic activity toward the oxygen evolution reaction (OER), many of them suffer from low stability at an anode current density in industrial scale. Herein, by combining a rapid epitaxial formation method with dynamic bubble-templated electrodeposition, we successfully developed single crystalline NiFeCu oxide catalysts with a hierarchical porous structure.

MicroRNA-181a-5p alleviates acute liver failure in mice by inhibiting HMGB1.

MicroRNAs (miRNAs) control liver diseases, but the role of microRNA-181a-5p in acute liver failure (ALF) is unclear. In this study, the ALF model was generated by injection of D-galactosamine (D-GalN) and lipopolysaccharide (LPS). The levels of miRNAs were assessed by microarray and qRT-PCR.