ABSTRACT
Aqueous zinc-ion batteries (AZIBs) exhibit promising prospects in becoming large-scale energy storage systems due to environmental friendliness, high security, and low cost. However, the growth of Zn dendrites and side reactions remain heady obstacles for the practical application of AZIBs. To solve these challenges, a functionalized Janus separator is successfully constructed by coating halloysite nanotubes (HNTs) on glass fiber (GF). Impressively, the different electronegativity on the inner and outer surfaces of HNTs endows the HNT-GF separator with ion-sieving property, leading to a significantly high transference number of Zn2+ (tZn2+ = 0.71). Meanwhile, the HNT-GF separator works as an interfacial ion comb to regular Zn2+ flux and realizes multisite progressive nucleation, bringing decreased nucleation overpotential and uniform Zn2+ deposition. Consequently, the HNT-GF separator enables the Zn anode to display an ultralong plating/stripping life of 3000 h and high rate tolerance with a stable long cycle life even under a density of 50 mA cm-2. Moreover, the Znâ¥HNT-GFâ¥MnO2 full cell represents an ultrastable cycling stability with a high capacity retention of 93.4% even after 1000 cycles at a current density of 2 A g-1. This work provides a convenient method for the separator modification of AZIBs.
ABSTRACT
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].
ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
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.
Subject(s)
Cymenes/pharmacology , Liver/injuries , Liver/metabolism , Protective Agents/pharmacology , Animals , Antigens, CD/metabolism , Blood Glucose , Cymenes/therapeutic use , Diabetes Mellitus, Experimental/pathology , Diabetes Mellitus, Type 2 , Insulin Receptor Substrate Proteins/metabolism , Insulin Resistance , Liver/pathology , Male , Mice , Mice, Inbred C57BL , Mice, Inbred Strains , NF-kappa B/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Proto-Oncogene Proteins c-akt , Receptor, Insulin/metabolism , Signal Transduction/drug effects , Toll-Like Receptor 4/metabolismABSTRACT
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.