Towards Superior Aqueous Zinc-Ion Batteries: The Insights of Artificial Protective Interfaces.

Aqueous zinc ion batteries (AZIBs) with metallic Zn anode have the potential for large-scale energy storage application due to their cost-effectiveness, safety, environmental-friendliness, and ease of preparation. However, the concerns regarding dendrite growth and side reactions on Zn anode surface hamper the commercialization of AZIBs. This review aims to give a comprehensive evaluation of the protective interphase construction and provide guidance to further improve the electrochemical performance of AZIBs. The failure behaviors of the Zn metal anode including dendrite growth, corrosion, and hydrogen evolution are analyzed. Then, the applications and mechanisms of the constructed interphases are introduced, which are classified by the material species. The fabrication methods of the artificial interfaces are summarized and evaluated, including the in-situ strategy and ex-situ strategy. Finally, the characterization means are discussed to give a full view for the study of Zn anode protection. Based on the analysis of this review, a stable and high-performance Zn anode could be designed by carefully choosing applied material, corresponding protective mechanism, and appropriate construction technique. Additionally, this review for Zn anode modification and construction techniques for anode protection in AZIBs may be helpful in other aqueous metal batteries with similar problems.

Na+ Preintercalated MoO3 Microrods for Aqueous Zinc/Sodium Batteries with Enhanced Performance.

Layered molybdenum trioxide (MoO3) is being investigated as a cathode material with high theoretical capacity and holds promise for aqueous secondary batteries. Unfortunately, the severe structural degradation of MoO3 and insufficient intrinsic properties hinder its practical application. Herein, a Na+ preintercalation strategy is reported as an effective method to construct cathodes with high performance for aqueous zinc/sodium batteries (AZSBs). Compared with pristine MoO3, the Na+ preintercalated Na0.25MoO3 cathode delivers a reversible capacity of 251.1 mAh g-1 at 1 A g-1, achieves a capacity retention of 79.2% after 500 cycles, and exhibits a high rate capability (121.5 mAh g-1 at 20 A g-1), which is superior to that in most of the previous reports. Through the experimental measurements and density functional theory (DFT) calculations, the preintercalation method could shorten the forbidden band gap and modulate the electronic structure and hence effectively inhibit the structural collapse of MoO3 microrods, induce reversible Na+ insertion, and enhance the discharge potential. This work is of significance for further research on molybdenum-based compounds as cathode materials for aqueous secondary batteries.

Tofacitinib Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury by Blocking the JAK-STAT1/STAT3 Signaling Pathway.

Septic acute kidney injury (AKI) is the most common AKI syndrome in the intensive care unit (ICU), and it accounts for approximately half of AKI cases. Tofacitinib (TOFA) is a pan-Janus kinase (JAK) inhibitor that exhibits potent anti-inflammatory activity in rheumatoid arthritis. However, no study has examined the functional role of TOFA in septic AKI. In the present study, we investigated the protective effects of TOFA on septic AKI and the underlying mechanisms. A lipopolysaccharide- (LPS-) induced AKI model was established in C57BL/6 mice via an intraperitoneal injection of LPS (10 mg/kg). One hour after LPS challenge, the mice were orally administered TOFA (5, 10, or 15 mg/kg) every 6 h until sacrifice at 24 h. We found that TOFA significantly ameliorated LPS-induced renal histopathological changes and dysfunction. TOFA also suppressed the expression levels of proinflammatory cytokines (TNF-α, IL-1ß, IL-6, and IFN-γ) and the parameters of oxidative stress (MDA, GSH, SOD, and CAT) in kidney tissues. These results may be associated with the inhibitory effect of TOFA on the JAK-STAT1/STAT3 pathway, which was significantly activated by LPS challenge. TOFA treatment also inhibited LPS-induced activation of the TLR4/NF-κB pathway. In conclusion, we revealed that TOFA had a protective effect on LPS-induced AKI, and it may be a promising therapeutic agent for septic AKI.

Matrine Suppresses Proliferation and Invasion of SGC7901 Cells through Inactivation of PI3K/Akt/uPA Pathway.

This study was to examine the inhibitory effect of matrine on the proliferation and metastasis of gastric cancer cells, and to explore the possible mechanisms involved in these processes. MTT was used to evaluate the proliferation ability of SGC7901 cells. A two and three-dimensional cell migration assay were performed to determine the effect of matrine on the migration of SGC7901 cells. Then, the changes of the uPA protein and other possible signal molecules were detected by western blot. We found that the proliferation ability of SGC 7901 cells was suppressed by matrine (p<0.05), and the average cell migration velocity was also significantly inhibited by matrine when compared to the control in a two-dimensional cell migration assay. In addition, SGC7901cells treated with matrine (50µg/ml) migrated less than the control cells in a three-dimensional cell migration assay. At the meantime, the decreased uPA protein expression in SGC7901 cells treated with matrine was observed, and the PI3K/Akt pathway was inhibited. These results suggested that matrine can inhibit the proliferation and metastasis of gastric cancer cells through the PI3K/Akt/uPA pathway, indicating that matrine might be a potential molecular target for treatment of gastric carcinoma.