Fast Ionic Conducting Hydroxyapatite Solid Electrolyte Interphase Enables Ultra-Stable Zinc Metal Anodes.

Zn metal has been extensively utilized as an anode in aqueous zinc-ion batteries attributed to its affordable cost and superior theoretical capacity. Nevertheless, the presence of dendrites and undesirable side reactions poses challenges to its widespread commercialization. To address these issues, herein, a surface coating composed of hydroxyapatite (HAP) was developed on the Zn anode to create an artificial solid electrolyte interphase. After the application of a hydroxyapatite layer, dendrites and corrosion of the Zn anode are sufficiently inhibited. Furthermore, the hydroxyapatite interphase with a low ionic diffusion barrier enables fast anodic redox kinetics. Consequently, the Zn@HAP symmetric cell possesses a durable lifespan over 2000 h at 1 mA cm-2, while maintaining minimal polarization. Moreover, the practical feasibilities of the Zn@HAP anode are also manifested in full batteries combined with MnO2 cathodes, exhibiting exceptional cycling performance up to 500 cycles at 1 A g-1 and excellent rate capability with a retention of 109 mAh g-1 at 5 A g-1.

[Corrigendum] Carvacrol may alleviate vascular inflammation in diabetic db/db mice.

Following the publication of the above article, the authors contacted the Editorial Office to explain that they made a couple of inadvertent errors in the assembly of the data panels showing the results of immunohistochemical experiments in Fig. 5K on p. 983 (the 'TLR4' experiments); essentially, the data panels selected for the '10 mg/mg Carvacrol' and '5 mg/kg Carvacrol' experiments were copied across from those shown for the 'NF­κB' experiments in the row above (Fig. 5I). The revised version of Fig. 5, showing the correct data for the'10 mg/mg Carvacrol' and '5 mg/kg Carvacrol' experiments in Fig. 5K, is shown on the next page. The authors can confirm that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 46: 977­988, 2020; DOI: 10.3892/ijmm.2020.4654].

Freestanding and Flexible Interfacial Layer Enables Bottom-Up Zn Deposition Toward Dendrite-Free Aqueous Zn-Ion Batteries.

Aqueous rechargeable zinc ion batteries are regarded as a competitive alternative to lithium-ion batteries because of their distinct advantages of high security, high energy density, low cost, and environmental friendliness. However, deep-seated problems including Zn dendrite and adverse side reactions severely impede the practical application. In this work, we proposed a freestanding Zn-electrolyte interfacial layer composed of multicapsular carbon fibers (MCFs) to regulate the plating/stripping behavior of Zn anodes. The versatile MCFs protective layer can uniformize the electric field and Zn2+ flux, meanwhile, reduce the deposition overpotentials, leading to high-quality and rapid Zn deposition kinetics. Furthermore, the bottom-up and uniform deposition of Zn on the Zn-MCFs interface endows long-term and high-capacity plating. Accordingly, the Zn@MCFs symmetric batteries can keep working up to 1500 h with 5 mAh cm-2. The feasibility of the MCFs interfacial layer is also convinced in Zn@MCFs||MnO2 batteries. Remarkably, the Zn@MCFs||α-MnO2 batteries deliver a high specific capacity of 236.1 mAh g-1 at 1 A g-1 with excellent stability, and maintain an exhilarating energy density of 154.3 Wh kg-1 at 33% depth of discharge in pouch batteries.

Protective effect of carvacrol on liver injury in type 2 diabetic db/db mice.

The present study aimed to investigate the protective effect of carvacrol on liver injury in mice with type 2 diabetes mellitus (T2DM) and to assess its potential molecular mechanism. Mice were divided into three groups (n=15/group): Non­diabetic db/m+ mice group, db/db mice group and db/db mice + carvacrol group. In the db/db mice + carvacrol group, db/db mice were administered 10 mg/kg carvacrol daily by gavage for 6 weeks. Fasting blood glucose and insulin levels were separately examined. Pathological changes were observed using hematoxylin and eosin, Masson's trichrome, periodic acid Schiff and reticular fiber staining. In addition, immunohistochemistry, immunofluorescence and western blotting were used to examine the expression levels of Toll­like receptor 4 (TLR4), NF­κB, NALP3, AKT1, phosphorylated (p)­AKT1, insulin receptor (INSR), p­INSR, mTOR, p­mTOR, insulin receptor substrate 1 (IRS1) and p­IRS1 in the liver tissues. The results revealed that carvacrol improved blood glucose and insulin resistance of T2DM db/db mice. After treatment with carvacrol for 6 weeks, the serum levels of TC, TG and LDL­C were markedly reduced, whereas HDL­C levels were significantly increased in db/db mice. Furthermore, carvacrol administration significantly decreased serum ALT and AST levels in db/db mice. Serum BUN, Cre and UA levels were markedly higher in db/db mice compared with those in the control group; however, carvacrol treatment markedly reduced their serum levels in db/db mice. Furthermore, histological examinations confirmed that carvacrol could protect the liver of db/db mice. Carvacrol could ameliorate liver injury induced by T2DM via mediating insulin, TLR4/NF­κB and AKT1/mTOR signaling pathways. The present findings suggested that carvacrol exerted protective effects on the liver in T2DM db/db mice, which could be related to insulin, TLR4/NF­κB and AKT1/mTOR signaling pathways.

Carvacrol may alleviate vascular inflammation in diabetic db/db mice.

Type 2 diabetes mellitus (T2DM) is associated with chronic low­grade inflammation. Carvacrol has been confirmed to possess anti­inflammatory properties, but its effect on diabetic vasculature remains unknown. The aim of the present study was to investigate the possible protective effects of carvacrol against vascular endothelial inflammation. The mice were divided into four groups (n=15 per group) as follows: Non­diabetic control mice, db/db mice, db/db mice + carvacrol (low) and db/db mice + carvacrol (high) groups. The effects of carvacrol on the pathomorphism of the thoracoabdominal aorta in db/db mice were evaluated using hematoxylin and eosin and Masson's trichrome staining. The serum levels of insulin signaling molecules, such as phosphorylated insulin receptor, phosphorylated insulin receptor substrate­1, insulin, triglyceride (TG) and inflammatory cytokines [tumor necrosis factor­α, interleukin (IL)­1ß, IL­6 and IL­8] were measured by ELISA. Furthermore, the protein levels of the toll­like receptor (TLR)4/nuclear factor (NF)­κB inflammatory signaling pathway molecules were investigated in the thoracoabdominal aorta of db/db mice and in high glucose­induced endothelial cells. Vascular endothelial cell apoptosis and viability were assessed by using flow cytometry and Cell Counting Kit­8 assays, respectively. The results demonstrated that carvacrol alleviated vascular endothelial cell injury. Carvacrol reduced the expression levels of insulin signaling molecules, insulin, TG and inflammatory cytokines in the serum of db/db mice. Moreover, carvacrol reduced the activation of the TLR4/NF­κB signaling pathway in vivo and in vitro. In vitro, carvacrol inhibited high glucose­induced endothelial cell function by promoting vascular endothelial cell apoptosis and suppressing cell viability. These findings demonstrated that carvacrol could alleviate endothelial dysfunction and vascular inflammation in T2DM.