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Soybean protein isolate (SPI)-stabilized nanoemulsions (NEs) were formulated to encapsulate diosgenin (DIO) to enhance its water solubility and bioavailability. The influence of DIO concentrations on NEs’ properties was investigated, and their environmental stability and cell permeability were also assessed. Results demonstrated that DIO significantly affected all the physicochemical properties of NEs. NEs with 1.0 mg/mL of DIO exhibited smaller droplet size (209 nm), lower polydispersity index (0.17), and higher stability coefficient (95.8 %). Furthermore, DIO-SPI NEs displayed better stability under appropriate pH ( 5), NaCl concentrations (≤0.3 M), temperatures (≤60 °C), and freeze–thaw cycles (≤2), as well as storage at 4 °C. Moreover, encapsulating DIO in NEs reduced its toxicity towards cells and enhanced its transport efficiency, which reached 3.16 ∼ 4.87 × 10−6. These findings highlight the potential of SPI-based NEs as a promising carrier for the efficient delivery of DIO.

Postbiotics are defined as "preparation of inanimate microorganisms and/or their components that confers a health benefit on the host". Postbiotics have unique advantages over probiotics, such as stability, safety, and wide application. Although postbiotics are research hotspots, the research on them is still very limited. This review provides comprehensive information on the scope of postbiotics, the preparation methods of inanimate microorganisms, and the application and mechanisms of postbiotics in metabolic syndrome (MetS). Furthermore, the application trends of postbiotics in the food industry are reviewed. It was found that postbiotics mainly include inactivated microorganisms, microbial lysates, cell components, and metabolites. Thermal treatments are the main methods to prepare inanimate microorganisms as postbiotics, while non-thermal treatments, such as ionizing radiation, ultraviolet light, ultrasound, and supercritical CO2, show great potential in postbiotic preparation. Postbiotics could ameliorate MetS through multiple pathways including the modulation of gut microbiota, the enhancement of intestinal barrier, the regulation of inflammation and immunity, and the modulation of hormone homeostasis. Additionally, postbiotics have great potential in the food industry as functional food supplements, food quality improvers, and food preservatives. In addition, the SWOT analyses showed that the development of postbiotics in the food industry exists both opportunities and challenges. [ABSTRACT FROM AUTHOR]

The low ionic conductivity, narrow electrochemical window, poor interfacial stability with lithium metal, and non-degradability of raw materials are the main problems of solid polymer electrolytes, restricting the development of lithium solid-state batteries. In this paper, a biodegradable poly (2,3-butanediol/1,3-propanediol/succinic acid/sebacic acid/itaconic acid) ester was designed and used as a substrate to prepare biodegradable polyester solid polymer electrolytes for solid-state lithium batteries using a simple solution-casting method. A large number of ester-based polar groups in the amorphous polymer become a high-speed channel for carrying lithium ions as a weak coordination site. The biodegradable polyester solid polymer electrolyte exhibits a wide electrochemical window of 5.08 V (vs. Li/Li+), high ionic conductivity of 1.03 mS cm−1 (25 °C), and a large Li+ transference number of 0.56. The electrolyte exhibits good interfacial stability with lithium, with stable Li plating/stripping behavior at room temperature over 2100 h. This design strategy for biodegradable polyester solid polymer electrolytes offers new possibilities for the development of matrix materials for environmentally friendly lithium metal solid-state batteries. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is a worldwide health problem with increasing incidence. Diosgenin (DIO) is a natural active ingredient extracted from Chinese yams (Rhizoma dioscoreae) with potential antioxidant, anti-inflammatory, and antidiabetic effects. However, the protective effect of DIO on DN is still unclear. The present study explored the mitigating effects and underlying mechanisms of DIO on DN in vivo and in vitro. In the current study, the DN rats were induced by a high-fat diet and streptozotocin and then treated with DIO and metformin (Mef, a positive control) for 8 weeks. The high-glucose (HG)-induced HK-2 cells were treated with DIO for 24 h. The results showed that DIO decreased blood glucose, biomarkers of renal damage, and renal pathological changes with an effect comparable to that of Mef, indicating that DIO is potential active substance to relieve DN. Thus, the protective mechanism of DIO on DN was further explored. Mechanistically, DIO improved autophagy and mitophagy via the regulation of the AMPK-mTOR and PINK1-MFN2-Parkin pathways, respectively. Knockdown of CaMKK2 abolished AMPK-mTOR and PINK1-MFN2-Parkin pathways-mediated autophagy and mitophagy. Mitophagy and mitochondrial dynamics are closely linked physiological processes. DIO also improved mitochondrial dynamics through inhibiting fission-associated proteins (DRP1 and p-DRP1) and increasing fusion proteins (MFN1/2 and OPA1). The effects were abolished by CaMKK2 and PINK1 knockdown. In conclusion, DIO ameliorated DN by enhancing autophagy and mitophagy and by improving mitochondrial dynamics in a CaMKK2-dependent manner. PINK1 and MFN2 are proteins that concurrently regulated mitophagy and mitochondrial dynamics. [ABSTRACT FROM AUTHOR]

Diosgenin (DIO) is a dietary steroid sapogenin possessing multiple biological functions, such as the amelioration of diabetes. However, the remission effect of DIO on diabetic nephropathy (DN) underlying oxidative stress and cell apoptosis remains unclear. Here, the effect of DIO on ROS generation and its induced cell apoptosis was studied in vitro and in vivo. Renal proximal tubular epithelial (HK-2) cells were treated with DIO (1, 2, 4 µM) under high glucose (HG, 30 mM) conditions. DN rats were induced by a high-fat diet combined with streptozotocin, followed by administration of DIO for 8 weeks. Our data suggested that DIO relieved the decline of HK-2 cell viability and renal pathological damage in DN rats. DIO also relieved ROS (O2− and H2O2) production. Mechanistically, DIO inhibited the expression of NOX4 and restored mitochondrial respiratory chain (MRC) complex I-V expressions. Further, DIO inhibited mitochondrial apoptosis by ameliorating mitochondrial membrane potential (MtMP) and down-regulating the expressions of CytC, Apaf-1, caspase 3, and caspase 9, while up-regulating Bcl2 expression. Moreover, the ER stress and its associated cell apoptosis were inhibited through decreasing PERK, p-PERK, ATF4, IRE1, p-CHOP, and caspase 12 expressions. Collectively, DIO inhibited ROS production by modulating NOX4 and MRC complexes, which then suppressed apoptosis regulated by mitochondria and ER stress, thereby attenuating DN. [ABSTRACT FROM AUTHOR]

Diosgenin (DIO) is a dietary and phytochemical steroidal saponin representing multiple activities. The present study investigated the protective effect of DIO on type II diabetes-associated nonalcoholic fatty liver disease (D-NAFLD). The rat model was established by high-fat diet and streptozotocin injection and then administered DIO for 8 weeks. The results showed that DIO reduced insulin resistance index, improved dyslipidemia, and relieved pancreatic damage. DIO decreased hepatic injury markers, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). H&E staining showed that DIO relieved hepatic lipid deposition. Mechanistically, DIO inhibited hepatic de novo lipogenesis (DNL) and increased fatty acid β-oxidation (FAO) through regulation of the AMPK-ACC/SREBP1 pathway. Endoplasmic reticulum (ER) stress was inhibited by DIO through regulation of PERK and IRE1 arms, which may then inhibit DNL. DIO also decreased reactive oxygen species (ROS) and enhanced the antioxidant capacity via an increase in Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx) activities. The mitochondria are the site for FAO, and ROS can damage mitochondrial function. DIO relieved mitochondrial fission and fusion disorder by inhibiting DRP1 and increasing MFN1/MFN2 expressions. Mitochondrial apoptosis was then inhibited by DIO. In conclusion, the present study suggests that DIO protects against D-NAFLD by inhibiting DNL and improving FAO and mitochondrial function. [ABSTRACT FROM AUTHOR]