Inhibition of SAT1 alleviates chondrocyte inflammation and ferroptosis by repressing ALOX15 expression and activating the Nrf2 pathway.

Aims: Osteoarthritis (OA) is the most common chronic pathema of human joints. The pathogenesis is complex, involving physiological and mechanical factors. In previous studies, we found that ferroptosis is intimately related to OA, while the role of Sat1 in chondrocyte ferroptosis and OA, as well as the underlying mechanism, remains unclear. Methods: In this study, interleukin-1ß (IL-1ß) was used to simulate inflammation and Erastin was used to simulate ferroptosis in vitro. We used small interfering RNA (siRNA) to knock down the spermidine/spermine N1-acetyltransferase 1 (Sat1) and arachidonate 15-lipoxygenase (Alox15), and examined damage-associated events including inflammation, ferroptosis, and oxidative stress of chondrocytes. In addition, a destabilization of the medial meniscus (DMM) mouse model of OA induced by surgery was established to investigate the role of Sat1 inhibition in OA progression. Results: The results showed that inhibition of Sat1 expression can reduce inflammation, ferroptosis changes, reactive oxygen species (ROS) level, and lipid-ROS accumulation induced by IL-1ß and Erastin. Knockdown of Sat1 promotes nuclear factor-E2-related factor 2 (Nrf2) signalling. Additionally, knockdown Alox15 can alleviate the inflammation-related protein expression induced by IL-1ß and ferroptosis-related protein expression induced by Erastin. Furthermore, knockdown Nrf2 can reverse these protein expression alterations. Finally, intra-articular injection of diminazene aceturate (DA), an inhibitor of Sat1, enhanced type II collagen (collagen II) and increased Sat1 and Alox15 expression. Conclusion: Our results demonstrate that inhibition of Sat1 could alleviate chondrocyte ferroptosis and inflammation by downregulating Alox15 activating the Nrf2 system, and delaying the progression of OA. These findings suggest that Sat1 provides a new approach for studying and treating OA.

DMT1-mediated iron overload accelerates cartilage degeneration in Hemophilic Arthropathy through the mtDNA-cGAS-STING axis.

INTRODUCTION: Excess iron contributes to Hemophilic Arthropathy (HA) development. Divalent metal transporter 1 (DMT1) delivers iron into the cytoplasm, thus regulating iron homeostasis. OBJECTIVES: We aimed to investigate whether DMT1-mediated iron homeostasis is involved in bleeding-induced cartilage degeneration and the molecular mechanisms underlying iron overload-induced chondrocyte damage. METHODS: This study established an in vivo HA model by puncturing knee joints of coagulation factor VIII gene knockout mice with a needle, and mimicked iron overload conditions in vitro by treatment of Ferric ammonium citrate (FAC). RESULTS: We demonstrated that blood exposure caused iron overload and cartilage degeneration, as well as elevated expression of DMT1. Furthermore, DMT1 silencing alleviated blood-induced iron overload and cartilage degeneration. In hemophilic mice, articular cartilage degeneration was also suppressed by intro-articularly injection of DMT1 adeno-associated virus 9 (AAV9). Mechanistically, RNA-sequencing analysis indicated the association between iron overload and cGAS-STING pathway. Further, iron overload triggered mtDNA-cGAS-STING pathway activation, which could be effectively mitigated by DMT1 silencing. Additionally, we discovered that RU.521, a potent Cyclic GMP-AMP Synthase (cGAS) inhibitor, successfully suppressed the downward cascades of cGAS-STING, thereby protecting against chondrocyte damage. CONCLUSION: Taken together, DMT1-mediated iron overload promotes chondrocyte damage and murine HA development, and targeted DMT1 may provide therapeutic and preventive approaches in HA.

Erratum: Mitoquinone alleviates osteoarthritis progress by activating the NRF2-Parkin axis.

[This corrects the article DOI: 10.1016/j.isci.2023.107647.].

Effects of oregano essential oil Pickering emulsion and ZnO nanoparticles on the properties and antibacterial activity of konjac glucomannan/carboxymethyl chitosan nanocomposite films.

Green and environmentally friendly natural bio-based food packaging films are increasingly favored by consumers. This study incorporated carboxylated-cellulose nanocrystal stabilized oregano essential oil (OEO) Pickering emulsion and ZnO nanoparticles (ZNPs) into konjac glucomannan (KGM)/carboxymethyl chitosan (CMCS) complexes to develop active food packaging films. The effects of OEO Pickering emulsion and ZNPs on the physical, structural, and antimicrobial activities of the nanocomposite films were evaluated. The OEO Pickering emulsion had a droplet size of 48.43 ± 3.56 µm and showed excellent dispersion and stability. Fourier transform infrared and X-ray diffraction analyses suggested that the interactions between the Pickering emulsion, ZNPs and KGM/CMCS matrix were mainly through hydrogen bonding. SEM observations confirmed that the Pickering emulsion and ZNPs were well incorporated into the KGM/CMCS matrix, forming tiny pores within the nanocomposite films. The incorporation of the OEO Pickering emulsion and/or ZNPs obviously increased the light and water vapor barrier ability, thermal stability, mechanical strength and antimicrobial properties of the KGM/CMCS nanocomposite film. Notably, KGM/CMCS/ZNPs/OEO Pickering emulsion films exhibited the highest barrier, and mechanical and antimicrobial activities due to the synergistic effect between the OEO Pickering emulsion and ZNPs. These results suggest that KGM/CMCS/ZNPs/OEO Pickering emulsion films can be utilized as novel active food packaging materials to extend the shelf life of packaged foods.

The attenuating effect of fermented soymilk on DSS-induced colitis in mice by suppressing immune response and modulating gut microbiota.

Fermented soymilk (FSM) as a new plant-based yoghurt has attracted attention for its nutritional and health benefits. The aim of this research is to explore the effect of consuming FSM before and during inflammatory bowel disease (IBD) on intestinal immune response, and to assess whether fermentation and sucrose can improve the anti-inflammatory activity of soymilk (SM) and FSM, and finally clarify their effect on the gut microbiota and levels of short-chain fatty acids (SCFAs). Consuming FSM in advance can effectively alleviate weight loss and bloody stools in mice with colitis and is associated with a 27% colon length repair rate. It can also prevent spleen and liver enlargement, inhibit immune response and oxidative stress, and increase the expression of the tight junction protein occludin gene (60%). Meanwhile, intaking FSM during IBD reduced weight loss, prevented liver damage, and repaired colon injury. In addition, fermentation enhance the inhibitory effects of FSM on colitis, whereas adding 3% sucrose to FSM had no effect on its intervention in colitis. Analysis of the composition of the gut microbiota in mice showed that the intake of FSM reduced the relative abundance of the pathogenic bacteria Parasutterella, Turicibater, and Bacteroide by 75%, 62%, and 50%, respectively, and increased the relative abundance of the beneficial bacteria Akkermansiaceae, Lachnospiraceae, Alloprevotella, and Dubosella by 28%, 50%, 80%, and 63%, respectively. It further restored the levels of SCFAs in the mouse intestine. The results provide a scientific basis for FSM as a natural anti-inflammatory food that can improve inflammatory intestinal microbiota imbalance and promote gut health.

P21 resists ferroptosis in osteoarthritic chondrocytes by regulating GPX4 protein stability.

Ferroptosis is involved in the pathogenesis of osteoarthritis (OA) while suppression of chondrocyte ferroptosis has a beneficial effect on OA. However, the molecular mechanism of ferroptosis in OA remains to be elucidated. P21, an indicator of aging, has been reported to inhibit ferroptosis, but the relationship between P21 and ferroptosis in OA remains unclear. Here, we aimed to investigate the expression and function of P21 in OA chondrocytes, and the involvement of P21 in the regulation of ferroptosis in chondrocytes. First, we demonstrated that high P21 expression was observed in the cartilage from OA patients and destabilized medial meniscus (DMM) mice, and in osteoarthritic chondrocytes induced by IL-1ß, FAC and erastin. P21 knockdown exacerbated the reduction of Col2a1 and promoted the upregulation of MMP13 in osteoarthritic chondrocytes. Meanwhile, P21 knockdown exacerbated cartilage degradation in DMM-induced OA mouse models and decreased GPX4 expression in vivo. Furthermore, P21 knockdown sensitized chondrocytes to ferroptosis induced by erastin, which was closely associated with the accumulation of lipid peroxides. In mechanism, we demonstrated that P21 regulated the stability of GPX4 protein, and the regulation was independent of NRF2. Meanwhile, we found that P21 significantly affected the recruitment of GPX4 to linear ubiquitin chain assembly complex (LUBAC) and regulated the level of M1-linked ubiquitination of GPX4. Overall, our results suggest that P21 plays an essential anti-ferroptosis role in OA by regulating the stability of GPX4.

Enhanced stabilization of multifunctional phenolic acids-grafted chitin nanofibers for Pickering emulsions.

The objective of this study was to develop novel functional stabilizers for Pickering emulsions using phenolic acids-grafted chitin nanofibers (phenolic acids-g-ChNF), which were fabricated by grafting ferulic acid (FA), sinapic acid (SA) and caffeic acid (CA) onto ChNF via free radical-mediated method. The Fourier transform infrared spectrum and Proton nuclear magnetic resonance showed that graft copolymerization occurred between the amino groups of ChNF and the carbonyl of the phenolic acids. Further, it was revealed that CA-g-ChNF and SA-g-ChNF possessed stronger antioxidant and antibacterial properties than the original ChNF and FA-g-ChNF. Additionally, we applied phenolic acids-g-ChNF to develop Pickering emulsions and found that SA-g-ChNF- and CA-g-ChNF-stabilized emulsions displayed reduced droplet sizes compared to FA, the main reason for which was that SA and CA had a rather close bonding relationship with ChNF. Taken together, SA-g-ChNF and CA-g-ChNF as novel multi-functional particles can be employed for facilitating the stability of Pickering emulsions.

Mitoquinone alleviates osteoarthritis progress by activating the NRF2-Parkin axis.

Osteoarthritis (OA) is a prevalent degenerative disease of the elderly. The NRF2 antioxidant system plays a critical role in maintaining redox balance. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant. This research aimed to determine whether MitoQ alleviated OA and the role of the NRF2/Parkin axis in MitoQ-mediated protective effects. In interleukin (IL)-1ß-induced OA chondrocytes, MitoQ activated the NRF2 pathway, reducing extracellular matrix (ECM) degradation and inflammation. MitoQ also increased glutathione peroxidase 4 (GPX4) expression, leading to decreased levels of reactive oxygen species (ROS) and lipid ROS. Silencing NRF2 weakened MitoQ's protective effects, while knockdown of Parkin upregulated the NRF2 pathway, inhibiting OA progression. Intra-articular injection of MitoQ mitigated cartilage destruction in destabilized medial meniscus (DMM)-induced OA mice. Our study demonstrates that MitoQ maintains cartilage homeostasis in vivo and in vitro through the NRF2/Parkin axis. We supplemented the negative feedback regulation mechanism between NRF2 and Parkin. These findings highlight the therapeutic potential of MitoQ for OA treatment.

Lipid peroxidation in osteoarthritis: focusing on 4-hydroxynonenal, malondialdehyde, and ferroptosis.

Osteoarthritis (OA) is a multifactorial and increasingly prevalent degenerative disease that affects the whole joint. The pathogenesis of OA is poorly understood and there is a lack of therapeutic interventions to reverse the pathological process of this disease. Accumulating studies have shown that the overproduction of reactive oxygen species (ROS) and ROS-induced lipid peroxidation are involved in the pathogenesis of OA. 4-Hydroxy-2-nonenal (4-HNE) and malondialdehyde (MDA) have received considerable attention for their role in cartilage degeneration and subchondral bone remodeling during OA development. Ferroptosis is a form of cell death characterized by a lack of control of membrane lipid peroxidation and recent studies have suggested that chondrocyte ferroptosis contributes to OA progression. In this review, we aim to discuss lipid peroxidation-derived 4-HNE and MDA in the progression of OA. In addition, the therapeutic potential for OA by controlling the accumulation of lipid peroxidation and inhibiting chondrocyte ferroptosis are discussed.

Corrigendum: Deferoxamine alleviates osteoarthritis by inhibiting chondrocyte ferroptosis and activating the Nrf2 pathway.

[This corrects the article DOI: 10.3389/fphar.2022.791376.].

Mechanism of the glucono-δ-lactone induced soymilk gelation: Enthalpy and entropy transformation in the cross-linking of protein molecules.

This study aimed to explore new techniques to regulate the quality of soy products. The glucono-δ-lactone (GDL) induced soymilk gelation process and the gel network structure characteristic were compared as a matter of temperature, and the role of reaction kinetics was discussed. Results showed that there were similarities in the development of G' curves under different temperatures, whereas the gel network structures and the energy requirements of cross-linking reactions were different. In the high-temperature region (70 °C-95 °C), the exposure and binding of reactive groups were promoted. The activation enthalpy (ΔH*) required by protein aggregates decreased and the effect of entropy reduction (-TΔS*) was enhanced, which led to shorten the preaggregation time (tg) and increase the gelation rate (k), resulting in the formation of rough, porous gel network with high stiffness. By contrast, in the low-temperature region (40 °C-70 °C), high enthalpy contributions and low entropy changes were required, then a fine, soft, and tender gel network formed. Besides, a funnel-shaped model of the enthalpy-entropy energy transformation mechanism of soymilk gelation was proposed. The results of this study revealed that adjusting the enthalpy-entropy energy requirements of the protein cross-linking reaction could be utilized to the regulation of the network structure and quality of soymilk gels, which could enrich the reaction kinetics theory and provide innovative ideas for food quality control technology from the perspective of energy requirement and energy input.

JNK-JUN-NCOA4 axis contributes to chondrocyte ferroptosis and aggravates osteoarthritis via ferritinophagy.

Interruption of iron homeostasis is correlated with cell ferroptosis and degenerative diseases. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy has been reported as a vital mechanism to control cellular iron levels, but its impact on osteoarthritis (OA) pathology and the underline mechanism are unknown. Herein we aimed to investigate the role and regulatory mechanism of NCOA4 in chondrocyte ferroptosis and OA pathogenesis. We demonstrated that NCOA4 was highly expressed in cartilage of patients with OA, aged mice, post-traumatic OA mice, and inflammatory chondrocytes. Importantly, Ncoa4 knockdown inhibited IL-1ß-induced chondrocyte ferroptosis and extracellular matrix degradation. Contrarily, overexpression of NCOA4 promoted chondrocyte ferroptosis and the delivery of Ncoa4 adeno-associated virus 9 into knee joint of mice aggravated post-traumatic OA. Mechanistic study revealed that NCOA4 was upregulated in a JNK-JUN signaling-dependent manner in which JUN could directly bind to the promoter of Ncoa4 and initial the transcription of Ncoa4. NCOA4 could interact with ferritin and increase autophagic degradation of ferritin and iron levels, which caused chondrocyte ferroptosis and extracellular matrix degradation. In addition, inhibition of JNK-JUN-NCOA4 axis by SP600125, a specific inhibitor of JNK, attenuated development of post-traumatic OA. This work highlights the role of JNK-JUN-NCOA4 axis and ferritinophagy in chondrocyte ferroptosis and OA pathogenesis, suggesting this axis as a potential target for OA treatment.

Inhibition of TRADD ameliorates chondrocyte necroptosis and osteoarthritis by blocking RIPK1-TAK1 pathway and restoring autophagy.

Osteoarthritis (OA) is an age-related disease characterized by cartilage degeneration. TNFR1-associated death domain protein (TRADD) is a key upstream molecule of TNF-α signals but its role in OA pathogenesis is unknown. This study aimed to verify that whether inhibition of TRADD could protect against chondrocyte necroptosis and OA, and further elucidate the underlying mechanism. We demonstrated that TNF-α-related OA-like phenotypes including inflammation response, extracellular matrix degradation, apoptosis, and necroptosis in chondrocytes were inhibited by TRADD deficiency. Furthermore, TRADD interacted with TRAF2 and knockdown of TRADD suppressed the activation of RIPK1-TAK1-NF-κB signals and restored impaired autophagy. ICCB-19, the selective inhibitor of TRADD, also attenuated necroptosis in chondrocytes. Mechanismly, ICCB-19 blocked the phosphorylation of TAK1-NF-κB signals and restored impaired autophagy, whereas inhibiting autophagic process with 3-Methyladenine compromised these effects of ICCB-19. The in vivo study showed that the intra-articular injection of ICCB-19 rescued the expression of collagen alpha-1(II) chain and LC3, and mitigated the cartilage degeneration of OA mice. This study demonstrates that TRADD mediates TNF-α-induced necroptosis and OA-like phenotypes of chondrocytes and suggests that ICCB-19 suppresses chondrocyte damage and cartilage degeneration by inhibiting TNF-α-TRADD-mediated signals and dysregulation of autophagy in chondrocytes. ICCB-19 may serve as an important option for OA therapy.

Preparation, characterization and biological activity of phosphorylated surface deacetylated chitin nanofibers.

Phosphorylation is a key route to achieve varieties of biological activities for polysaccharides. Here, we report the phosphorylated surface deacetylated chitin nanofibers (PS-ChNFs) using the sodium tripolyphosphate/sodium trimetaphosphate (STPP/STMP) method. Response surface methodology (RSM) was employed to optimize in this study. Under optimal conditions, a maximum degree of substitution (DS) of 0.13 was obtained. In addition, the structures of PS-ChNFs were investigated by Fourier transform infrared spectroscopy (FT-IR), Nuclear Magnetic Resonance spectra (NMR), X-ray photoelectron spectroscopy (XPS), Scanning electron microscope (SEM) and (Energy Dispersive Spectroscopy-mapping) EDS-mapping. The findings revealed that the FT-IR spectroscopy and XPS analysis confirmed the appearance of phosphate groups in PS-ChNFs. The 31P NMR results indicate that the PS-ChNFs structure has characteristic peaks of P elements. SEM images showed that PS-ChNFs had a rough surface with many cavities, but the P elements on the surface of the EDS-mapping are uniformly distributed throughout the sample without any enrichment. Antioxidant and antibacterial test showed that PS-ChNFs had significant scavenging effect on free radicals and antibacterial effect. The above results indicate that the chemical modification of PS-ChNFs was successful.

Succession and Diversity of Microbial Flora during the Fermentation of Douchi and Their Effects on the Formation of Characteristic Aroma.

This study aims to understand the development and succession of the microbial community during the production of traditional Aspergillus-type Douchi as well as their effects on the formation and variation of characteristic aroma compounds. High-throughput sequencing technology, solid-phase microextraction, gas chromatography-mass spectrometry, and Spearman correlation analysis were conducted to study the changes in the microbial community and characteristic flavor during the fermentation process. Aspergillus spp. was dominant in the early stage of fermentation, whereas Staphylococcus spp., Bacillus spp., and Millerozyma spp. became dominant later. At the early stage, the main flavor compounds were characteristic soy-derived alcohols and aldehydes, mainly 1-hexanol, 1-octen-3-ol, and nonanal. In the later stage, phenol, 2-methoxy-, and 3-octanone were formed. Correlation analysis showed that six bacterial genera and nine fungal genera were significantly correlated with the main volatile components, with higher correlation coefficients, occurring on fungi rather than bacteria. Alcohols and aldehydes were highly correlated with the relative abundance of bacteria, while that of yeast species such as Millerozyma spp., Kodamaea spp., and Candida spp. was positively correlated with decanal, 3-octanol, 2-methoxy-phenol, 4-ethyl-phenol, 3-octanone, and phenol. The novelty of this work lies in the molds that were dominant in the pre-fermentation stage, whereas the yeasts increased rapidly in the post-fermentation stage. This change was also an important reason for the formation of the special flavor of Douchi. Correlation analysis of fungi and flavor substances was more relevant than that of bacteria. As a foundation of our future focus, this work will potentially lead to improved quality of Douchi and shortening the production cycle by enriching the abundance of key microbes.

Desferoxamine protects against hemophilic arthropathy through the upregulation of HIF-1α-BNIP3 mediated mitophagy.

AIMS: Hemophilic arthropathy (HA) is a typically iron overload induced joint disease secondary to continuous joint bleeding, however, the exact role of iron chelators in HA has not been fully elucidated. In the present study, we investigated whether desferoxamine (DFO), an iron chelator, could limit the development of HA and the underlying mechanisms. MATERIALS AND METHODS: A HA mice model was established by needle puncture in the left knees of FVIII-deficient hemophilic mice. HA progression was evaluated at 8 weeks after DFO administration. Moreover, chondrocytes were treated with ferric ammonium citrate (FAC) to mimic iron overload in vitro. Modulating effect of DFO on iron overload induced oxidative stress, chondrocytes apoptosis and extracellular matrix (ECM) degradation and the role of HIF-1α-BNIP3 mediated mitophagy were examined. KEY FINDINGS: We found that DFO limited the development of HA and protected iron overload induced ECM degradation, chondrocytes apoptosis and oxidative stress. Besides chelating Fe2+, we found that HIF-1α-BNIP3 mediated mitophagy played important roles in the protective effect of DFO. HIF-1α inhibition suppressed chondrocytes mitophagy process and partly diminished the protective effect of DFO on chondrocytes iron overload. SIGNIFICANCE: In conclusion, DFO could protect against HA development via HIF-1α-BNIP3 mediated mitophagy, suggesting DFO might be a potential therapeutic supplement for HA treatment.

Indirubin protects chondrocytes and alleviates OA by inhibiting the MAPK and NF-κB pathways.

PHARMACOLOGICAL RELEVANCE: Indirubin (IR) is a key active ingredient in the traditional Chinese medication QingDai, also called indigo naturalis, which are extensively used in China to treat chronic diseases, such as inflammation and cancer. However, the function of IR in reducing chondrocyte inflammation in osteoarthritis (OA) is still unclear. AIM OF THE STUDY: The aim of this research was to examine how IR inhibits arthritis and to highlight some of its cellular-level processes. MATERIALS AND METHODS: Chondrocytes from the knee joint of C57 mice were gathered and grown for in vitro tests and used to determine the toxicity of IR toward chondrocytes using a CCK8 kit. Chondrocytes were treated with IL-1ß and IR or with IL-1ß alone, and western blotting was used to determine the expression levels of inflammatory mediators. Meanwhile, through the identification and examination of pertinent markers via quantitative PCR. By using PCR assays, western blotting, toluidine blue staining and safranin O staining, the expression of proteoglycan (AGG) and type II collagen (collagen II) was investigated. Furthermore, western blotting was used to detect activation of the NF-κB and MAPK signaling pathways, and immunofluorescence was used to detect p65 nuclear translocation. In an in vivo experiment, C57BL/6 mice were subjected to destabilization of the medial meniscus (DMM) surgery to produce an OA model, and IR was injected into the articular cavity for 8 weeks. Eventually, the mice were killed, and samples of the knee joints were obtained for histological examination and analysis. RESULTS: IR significantly reduced the expression of inflammatory regulators in chondrocytes treated with IL-1ß, including iNOS and COX-2. Inhibition of IL-1ß induced production of the key catabolic enzymes MMP3, MMP13 and A5. Additionally, an improvement in the downregulation of collagen II and AGG expression was observed. Moreover, IR prevented the aberrant IL-1ß-induced activation of the NF-κB and MAPK signaling pathways, which resulted in downregulation of p65 and p38 expression. Compared to the DMM group, the severity of cartilage injury in animals was dramatically lessened and OARSI scores were lower in the treated groups. CONCLUSION: According to the above findings, IR is quite effective in preventing arthritis both in vivo and in vitro, suggesting that IR may be employed as a possible anti-arthritis drug.

Micro-structure and tensile properties of microfluidic spinning konjac glucomannan and sodium alginate composite bio-fibers regulated by shear and elongational flow: experiment and multi-scale simulation.

Microfluidic spinning has been widely used to produce bio-fibers with excellent tensile performances by regulating the conformation of biological macromolecules. However, the effect of channel shapes on fiber tensile performances is unclear. In this study, bio-fibers were prepared using konjac glucomannan and sodium alginate by five channels. The micro-morphology and tensile performance of fibers were characterized and measured. Then, the dynamical behaviours of macromolecule clusters in flow fields were simulated by multi-scale numerical methods. The results show that the elongational flow with increasing extension rates produced fibers with a tensile strength of 32.34 MPa and a tensile strain of 18.72 %, which were 1.37 and 1.55 times that for a shear flow, respectively. The difference in tensile performances was attributed to the micro-morphology regulated by flow fields. The continuously increasing extension rate of flow was more effective than the shear rate or the maximum extension rate for the stretching of macromolecule clusters. We conclude that the channel shapes significantly influence flow fields, dynamical behaviours of molecule clusters, the morphology of fibers, and tensile performances. This study provides a novel numerical method and understanding of microfluidic spinning, which will promote the optimization and applications of bio-fibers.

Oxidized Chitin Nanocrystals Greatly Strengthen the Stability of Resveratrol-Loaded Gliadin Nanoparticles.

Resveratrol (RES) is a natural polyphenol with a variety of health beneficial properties, but its application is greatly limited due to low aqueous solubility and poor bioavailability. This study aims to address these issues via gliadin nanoparticles stabilized with oxidized chitin nanocrystals (O-ChNCs) as a delivery system for RES. RES-loaded gliadin nanoparticles (GRNPs) were fabricated by an antisolvent method, and their formation mechanism was elucidated using zeta-potential, FTIR, XRD, and TEM. Furthermore, the effect of O-ChNCs on the colloidal stability and bioactiveness of GRNPs was discussed. The results demonstrate that O-ChNCs are adsorbed onto the surface of GRNPs through hydrogen bonding and electrostatic interactions, leading to the enhanced absolute potential and the improved hydrophobicity of the particles, which in turn facilitates the stability of the GRNPs. Furthermore, the changes in the release profile and antioxidant activity of RES in the simulated gastric and intestinal tracts indicate that the adsorption of O-ChNCs not only delays the release of RES but also has a protective effect on the antioxidant capacity of RES. This study provides significant implications for developing stable gliadin nanoparticles as delivery vehicles for bioactive substances.

Properties of AgSnO2 Contact Materials Doped with Different Concentrations of Cr.

As an important component carrying the core function and service life of switching appliances, the selection and improvement of electrical contact materials is of great significance. AgSnO2, which is non-toxic, environmentally friendly and has excellent performance, has become the most promising contact material to replace AgCdO. However, it has deficiencies in machinability and electrical conductivity. The property of AgSnO2 contact material was improved by doping element Cr. The relationship between the mechanical and electrical properties of AgSnO2 contact materials and doping concentrations were investigated and analyzed by simulation and experiment. Based on the first principle, the elastic constants of supercell models Sn1-xCrxO2 (x = 0, 0.083, 0.125, 0.167, 0.25) were calculated. The results show that the material with a doping ratio of 25% is least prone to warp and crack, and the material with a doping ratio of 12.5% has the best toughness and ductility and the lowest hardness, which leads to molding and is subsequently easier to process. The Cr-doped AgSnO2 contacts with different doping proportions were prepared by the sol-gel and powder metallurgy method. Additionally, their physical performance and electrical contact properties were measured in experiments. The results show that the doped SnO2 powders prepared by the sol-gel method realize integration doping, which is consistent with the crystal model constructed in the simulation calculation. Sn0.875Cr0.125O2 has lower hardness, which is beneficial to process and form. Doping helps to stabilize the arc root, inhibit the ablation of contact by arc, reduces arc duration and arc energy, improves the resistance to arc erosion of AgSnO2 contact material, and makes electrical contact performance more stable. The contact material with a doping concentration of 16.7% has the best arc erosion resistance.