Preparation of Low-Defect Manganese-Based Prussian Blue Cathode Materials with Cubic Structure for Sodium-Ion Batteries via Coprecipitation Method.

Sodium-ion batteries have important application prospects in large-scale energy storage due to their advantages, such as safety, affordability, and abundant resources. Prussian blue analogs (PBAs) have a stable and open framework structure, making them a very promising cathode material. However, high-performance manganese-based Prussian blue cathode materials for sodium-ion batteries still suffer from significant challenges due to several key issues, such as a high number of vacancy defects and a high crystal water content. This article investigates the effects of the Fe-Mn molar ratio, Mn ion concentration, and reaction time on the electrochemical performance of MnHCF during the coprecipitation process. When Fe:Mn = 1:2, c(Mn2+) = 0.02 mol/L, and the reaction time is 12 h, the content of interstitial water molecules in the sample is low, and the Fe(CN)6 defects are few. At 0.1 C, the prepared electrode has a high initial discharge specific capacity (121.9 mAh g-1), and after 100 cycles at 0.2 C, the capacity retention rate is 65% (~76.2 mAh g-1). Meanwhile, the sample electrode exhibits excellent reversibility. The discharge capacity can still be maintained at around 75% when the magnification is restored from 5 C to 0.1 C. The improvement in performance is mainly attributed to two aspects: On the one hand, reducing the Fe(CN)6 defects and crystal water content is conducive to the diffusion and stable structure of N. On the other hand, reducing the reaction rate can significantly delay the crystallization of materials and optimize the nucleation process.

Cardamonin targets KEAP1/NRF2 signaling for protection against atherosclerosis.

Atherosclerosis (AS)-induced cardiovascular disease is a leading cause of death worldwide. To date, there is still a lack of effective approaches for AS intervention. Cardamonin (CAD) is a bioactive food component, but its effect on AS is unknown. In this work, CAD was investigated for its effect on AS using low-density lipoprotein receptor knockout mice and tumor necrosis factor-alpha (TNF-α)-stimulated endothelial cells (ECs). After a 12-week intervention, CAD was found to significantly prevent AS formation in the aortic root and aortic tree, reduce the necrotic core area, and inhibit aortic inflammation and oxidative stress. Moreover, CAD quenched TNF-α-provoked inflammation and oxidative stress in ECs. RNA-sequencing identified nuclear factor erythroid-2 related factor 2 (NFE2L2, NRF2)/heme oxidase 1 (HO1) signaling to be drastically activated by CAD. CAD is a known activator of the aryl hydrocarbon receptor (AHR) which is a transcription factor of the NFE2L2 gene. Surprisingly, AHR was not required for CAD's action on the activation of NRF2/HO1 signaling since AHR gene silencing did not reverse this effect. Furthermore, a molecular docking assay showed a strong binding potential of CAD to the Kelch domain of the Kelch-like ECH-associated protein 1 (KEAP1) which sequesters NRF2 in the cytoplasm. Both CAD and the Kelch domain inhibitor Ki696 promoted NRF2 nuclear translocation, whereas the combination of CAD and Ki696 did not yield a greater effect compared with either CAD or Ki696, confirming the interaction of CAD with the Kelch domain. This work provides an experimental basis for CAD as a novel and effective bioactive food component in future AS interventions.

Local Application of Krill Oil Accelerates the Healing of Artificially Created Wounds in Diabetic Mice.

Diabetes mellitus (DM) impairs the wound healing process, seriously threatening the health of the diabetic population. To date, few effective approaches have been developed for the treatment of diabetic wounds. Krill oil (KO) contains bioactive components that have potent anti-inflammatory and anti-oxidative activities. As prolonged inflammation is a crucial contributor to DM-impaired wound healing, we speculated that the local application of KO would accelerate diabetic wound healing. Therefore, KO was applied to artificially created wounds of type 2 diabetic mice induced by streptozotocin and high-fat diet. The diabetic mice had a delayed wound healing process compared with the non-diabetic control mice, with excessive inflammation, impaired collagen deposition, and depressed neovascularization in the wound area. These effects were dramatically reversed by KO. In vitro, KO blocked the TNF-α-induced macrophage inflammation, fibroblast dysfunction, and endothelial angiogenic impairment. The present study in mice suggests that KO local application could be a viable approach in the management of diabetic wounds.

Krill Oil Turns Off TGF-ß1 Profibrotic Signaling in the Prevention of Diabetic Nephropathy.

Diabetic nephropathy (DN), a severe microvascular complication of diabetes mellitus (DM), results in high mortality due to the lack of effective interventions. The current study investigated the preventive effect of krill oil (KO) on DN using a type 2 DM mouse model induced by streptozotocin and high-fat diet for 24 weeks. The diabetic mice developed albuminuria, mesangial matrix accumulation, glomerular hypertrophy, and fibrosis formation, with an increase in renal proinflammatory, oxidative and profibrotic gene expression. KO significantly prevented these effects but did not improve hyperglycemia and glucose intolerance. In high-glucose-treated mesangial cells (MCs), KO preferably modulated TGF-ß1 signaling as revealed by RNA-sequencing. In TGF-ß1-treated MCs, KO abolished SMAD2/3 phosphorylation and nuclear translocation and activated Smad7 gene expression. The action of KO on the SMADs was confirmed in the diabetic kidneys. Therefore, KO may prevent DN predominantly by suppressing the TGF-ß1 signaling pathway.

Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications.

Gut microbiota has attracted widespread attention due to its crucial role in disease pathophysiology, including type 2 diabetes mellitus (T2DM). Metabolites and bacterial components of gut microbiota affect the initiation and progression of T2DM by regulating inflammation, immunity, and metabolism. Short-chain fatty acids, secondary bile acid, imidazole propionate, branched-chain amino acids, and lipopolysaccharide are the main molecules related to T2DM. Many studies have investigated the role of gut microbiota in T2DM, particularly those butyrate-producing bacteria. Increasing evidence has demonstrated that fecal microbiota transplantation and probiotic capsules are useful strategies in preventing diabetes. In this review, we aim to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders, the underlying mechanisms, and translational applications of gut microbiota. This review will provide novel insight into developing individualized therapy for T2DM patients based on gut microbiota immunometabolism.