No abstract

Hepatic injury provoked by cold storage is a major problem affecting liver transplantation, as exposure to cold induces apoptosis in hepatic tissues. Long noncoding RNAs (lncRNAs) are increasingly understood to regulate apoptosis, but the contribution of lncRNAs to cold-induced liver injury remains unknown. Using RNA-seq, we determined the differential lncRNA expression profile in mouse livers after cold storage and found that expression of the lncRNA TUG1 was significantly down-regulated. Overexpression of TUG1 attenuated cold-induced apoptosis in mouse hepatocytes and liver sinusoidal endothelial cells LSECs, in part by blocking mitochondrial apoptosis and endoplasmic reticulum (ER) stress pathways. Moreover, TUG1 attenuated apoptosis, inflammation, and oxidative stress in vivo in livers subjected to cold storage. Overexpression of TUG1 also improved hepatocyte function and prolonged hepatic graft survival rates in mice. These results suggest that the lncRNA TUG1 exerts a protective effect against cold-induced liver damage by inhibiting apoptosis in mice, and suggests a potential role for TUG1 as a target for the prevention of coldinduced liver damage in liver transplantation. DatabasesRNA-seq data are available from GEO using accession number GSE76609.

A single-atom dispersed Ni doping strategy to boost the performance of N–C materials for CO2RR by the pyrolysis of a metal–organic molecule complex was reported and revealed.

No abstract

Sodium (Na) metal as an anode is one of the ultimate choices for the high‐energy rechargeable batteries in virtue of its intrinsic high theoretical capacity (1166 mAh g−1) and low redox potential (−2.71V vs standard hydrogen electrode (SHE)), as well as its low cost and broad sources. Nevertheless, the dendrite‐related hazards seriously block its practical application. Na dendrite formation mainly emanates from the uncontrolled Na deposition behavior. Therefore, it seems particularly important to employ appropriate strategies towards the homogeneous deposition of Na for the dendrite‐free metal anode. In this review, the challenge of regulating Na homogeneous deposition for dendrite‐free Na anodes is first discussed. Then, recent advances in the strategies of regulating the Na uniform deposition are summarized, including adjusting Na+ flux near the solid‐liquid interface and improving sodiophilicity on the biphase interface. Lastly, perspectives on further research and important factors toward the practical application of high‐energy‐density Na metal batteries are emphasized in detail.

No abstract

Background Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown. This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms. Methods In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice. The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured. In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed. Results We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).

Acetaminophen (APAP) is one of the safest and most effective over-the-counter (OTC) analgesics and antipyretics, but excessive doses of which will induce hepatotoxicity with high morbidity and mortality worldwide. Kaempferol...