In this study, a sustainable, and recyclable antimicrobial food packaging film was fabricated. Polyvinyl alcohol (PVA), phytic acid (PA), and sodium silicate (Na2SiO3) were employed as green raw materials, and the films were prepared via a simple casting process. A key breakthrough is the in-situ synthesis of SiO2 nanoparticles in the PVA-PA matrix using Na2SiO3 as the precursor. The weakly acidic environment of the PVA-PA system (provided by PA's phosphate groups) promotes Na2SiO3 hydrolysis without additional acidifiers. This design avoids common issues in conventional hybrid films, such as SiO2 agglomeration and complex synthesis processes. Experimental results indicate that the optimized PSPII2 film exhibits exceptional comprehensive performance. Its mechanical strength, thermal stability, and antibacterial properties are remarkably enhanced through the synergistic crosslinking of PA and in-situ generated SiO2. The PSPII2 film exhibits significant antibacterial activity against E. coli and S. aureus. Practical storage tests confirm that it extends the shelf life of refrigerated chicken breast to 11 days while effectively reducing total volatile basic nitrogen (TVB-N) content. In addition, the film can dissolve in water at 90 degrees C, and after recovery, it can be remolded into new film. This can be remolded via a simple and green approach with well-retained performance, which reflects its excellent recyclability and sustainability. It also has good thermal compression processability for diverse packaging scenarios. In summary, PSPII2 film not only possesses outstanding functionality but also provides a new strategy for environmentally friendly packaging, demonstrating its great potential as a recyclable and sustainable food packaging material.

Myocardial ischemia-reperfusion injury (MIRI) remains a major clinical challenge due to limited therapeutic options and the risk of complications such as hemorrhage. Dihydromyricetin (DMY), a flavonoid derived from Vine tea, has shown cardioprotective effects, but its mechanism of action in MIRI is not fully understood. This study aimed to investigate the therapeutic effects of DMY on MIRI and elucidate the underlying molecular mechanisms. A rat model of MIRI was established by left anterior descending coronary artery ligation. Rats received DMY or the positive control diltiazem (DIL) for 7 days post-injury. Cardiac damage was assessed by measuring cardiac troponin levels and histopathological analysis. The expression of chemokine-like factor 1 (CKLF1) and its downstream signaling pathways was examined using molecular and biochemical approaches. The interaction between DMY and CKLF1 was further validated using a CKLF1 agonist (C27) and CKLF1-knockout rats. CKLF1 expression was significantly upregulated in MIRI, correlating with inflammatory infiltration, tissue disorganization, and elevated cardiac troponin levels. Mechanistically, CKLF1 activation promoted phosphorylation of nuclear factor kappa-B (NF-κB) and subsequent assembly of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome, leading to caspase-1-dependent pyroptosis. DMY treatment attenuated these effects by downregulating CKLF1 expression and disrupting its interaction with C-C chemokine receptor type 5 (CCR5) and NLRP3, thereby suppressing pyroptosis. Notably, activation of CKLF1 signaling by its agonist C27 reversed the protective effects of DMY. Moreover, while CKLF1 knockout modestly reduced pyroptosis-related protein expression, the anti-pyroptotic effect of DMY was abolished in knockout rats, indicating its dependence on CKLF1. These findings demonstrate that DMY alleviates MIRI by targeting the CKLF1/NF-κB/NLRP3 axis, thereby inhibiting pyroptosis and preserving cardiomyocyte integrity. The anti-pyroptotic effect of DMY is specifically dependent on CKLF1 expression. This study provides a novel mechanistic basis for developing targeted therapies against MIRI.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly serious global health issue. The establishment of accurate animal models is crucial for elucidating its pathogenesis and developing effective therapeutic strategies. Although mouse models are widely used in MASLD research, they exhibit significant differences from humans in metabolic traits and disease progression, limiting their ability to fully recapitulate key pathological features of MASLD. In this study, we established an MASLD model in Apodemus peninsulae using a high-fat diet (HFD) and compared it with the commonly used C57BL/6J mouse model. The results showed that A. peninsulae developed marked lipid metabolism disorders and liver function impairment as early as week 4 with an HFD intervention. Histological analysis revealed progressive steatosis, inflammatory infiltration, and early fibrosis from weeks 8 to 16, which was confirmed by oil red O, Masson's trichrome, and Sirius red staining. In contrast, pathological progression in C57Bl/6J mice was slower, with milder fibrosis. Immunolabeling and inflammatory cytokine expression further indicated a more intense inflammatory response in A. peninsulae. Overall, A. peninsulae offers advantages, such as rapid disease induction and stable phenotypes, making it a promising animal model for studying early-stage MASLD. Its shorter modeling period and more pronounced steatosis and liver injury suggest it more closely mimics the early pathological changes seen in human MASLD.

Gastric cancer (GC) is a major global digestive malignancy with high incidence and mortality. Circular fanconi anemia complementation group B (circFANCB) expression is elevated in cancer, and its suppression suppresses tumor progression. However, research on the function of circFANCB in GC has not been reported yet. The role and mechanism of circFANCB in GC were investigated through circular RNA (circRNA) sequencing, database prediction, and experimental validation, including quantitative real-time PCR (qRT-PCR), ribonuclease R assay, nuclear-cytoplasmic fractionation, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, wound healing assay, Transwell assay, tube formation assay, western blot, dual-luciferase reporter assay, and enzyme-linked immunosorbent assay. Furthermore, its mechanism was further explored in vivo using a xenograft nude mouse model and immunohistochemistry. Online prediction tools, methylation-dependent RNA immunoprecipitation (MeRIP), and RNA immunoprecipitation (RIP) assays were employed to investigate whether methyltransferase-like protein 3 (METTL3) targeted circular FANCB (circFANCB) via m6A methylation. In GC, circFANCB expression was upregulated. Knockdown of circFANCB inhibited cell proliferation, migration, invasion, and angiogenesis while promoting cell death. CircFANCB increased CEACAM5 expression by binding to miR-454-3p. CEACAM5 suppressed ferroptosis in GC cells. Rescue experiments confirmed that circFANCB inhibited ferroptosis by upregulating CEACAM5, thereby promoting GC cell proliferation. Animal models demonstrated that circFANCB knockdown inhibited GC tumor growth. Additionally, METTL3 enhanced circFANCB expression through m6A methylation. Rescue experiments further confirmed that METTL3 promotes the malignant phenotype of GC cells by upregulating circFANCB. The m6A-modified circFANCB promotes the malignant progression of GC by regulating ferroptosis via the miR-454-3p/CEACAM5 axis, providing a theoretical basis for potential clinical therapeutic strategies.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuronal loss and the accumulation of α-synuclein-containing Lewy bodies. Growing evidence indicates that neuroinflammation, particularly through the activation of Toll-like receptors (TLRs), contributes significantly to PD pathogenesis. TLRs, particularly TLR2 and TLR4, detect endogenous damage-associated molecular patterns such as misfolded α-synuclein. This recognition initiates signaling pathways that drive microglial activation, pro-inflammatory cytokine release, and oxidative stress, ultimately leading to neuronal injury. This review synthesizes current insights into TLR involvement in PD, highlighting their roles in linking innate and adaptive immune responses, regulating neuroinflammatory cascades, and mediating interactions across the gut-brain axis. Furthermore, we examine the therapeutic potential of plant-derived bioactive compounds-including flavonoids, terpenoids, polyphenols, alkaloids, and lignans-as natural TLR modulators. These phytochemicals have demonstrated neuroprotective effects in preclinical studies by attenuating TLR-mediated inflammatory responses, reducing oxidative stress, and improving motor and cognitive outcomes. Challenges such as target specificity, bioavailability, and translational applicability are also discussed, along with future directions for advancing TLR-focused phytochemical therapies. This review provides a theoretical and mechanistic framework supporting natural TLR modulators as promising disease-modifying strategies in PD.

Abstract Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by progressive cognitive decline. Tetrahydroxy stilbene glucoside (TSG) has been demonstrated to improve learning and memory in aged mice; however, its underlying mechanisms remain incompletely understood. This study aimed to elucidate the effects of TSG on cognitive impairment in APP/PS1 mice through analysis of gut microbiota and associated metabolites. Behavioral tests, immunohistochemistry, and 16S rDNA sequencing revealed that TSG treatment improved cognitive function and alleviated neuroinflammation. Furthermore, TSG restored gut microbiota homeostasis and normalized aberrant metabolite profiles, accompanied by elevated levels of short-chain fatty acids (SCFAs). Correlation analysis indicated associations between alterations in gut microbiota, metabolites, and SCFAs. Notably, TSG promoted the production and content of SCFAs, especially acetic acid, propionic acid, and hexanoic acid. These findings suggest that TSG mitigates AD-related pathology possibly via modulation of specific gut microbial communities and their metabolic outputs, providing a basis for further therapeutic exploration.

Polystyrene (PS), as a widely used plastic product, especially polystyrene foam (PSF), will permanently pollute the environment after consumption, the vast volume restricts its recycling and reuse. In this work, a novel environmentally friendly and sustainable approach is used to recycle waste PSF via near-critical water (NCW) method. Under NCW condition (185 +/- 10 degrees C, 1-1.5 MPa), the morphology of waste PSF changes to viscous state, returns to glassy state with subsequent temperature decrease, before finally recycling. The basic attributes of the recovered PS beads such as, chemical structure and thermal stability almost no change, which demonstrated the NCW method was feasible. This work proposes a new idea for recycling more pure PS, use water as the reaction medium reducing the use of organic solvent to protect environment, and reducing the CO2 emission of the PS traditional synthetic pathway, which effectively alleviating the consumption of non-renewable resources and has potential to be sustainable recycled, reused of solid waste resource and applied on a large scale.

Background One type of chronic kidney disease is diabetic nephropathy. One of the main causes of end-stage renal disease and chronic kidney disease is diabetic nephropathy. The objective of this study was to assess the effects of treating diabetic nephropathy with conessine extract on male wistar rats with diabetes that had been triggered by streptozotocin. Materials and Methods Twenty-four rats were split up into four groups. The regular diet was fed to the negative control animals in the first group. After receiving a single intravenous injection of streptozotocin to cause diabetes, the remaining 18 rats were split equally into three groups: the diabetic control group was placed in group 2, the third group received oral treatment with 20 mg/ kg of conessine, and the fourth group received oral treatment with 5 mg/kg of gliclazide. Results In comparison to the negative control, the rats in the second group had higher glucose and lipid peroxide levels and lower SOD, CAT, GR, GPx, and GSH activity. Diabetes also led to an increase in immunoglobulins, interleukin-6, and carboxymethyl lysine. Potassium and sodium levels were lowered, while kidney function metrics were also raised. renal tissues also displayed significant histological alterations. Conclusion Conessine treatments, administered to the diabetic rats in the third improved all altered biochemical and pathological tests that were getting closer to the negative control.

Tetrahydroxy stilbene glycoside (TSG), which is the primary active substance of Chinese herbal medicine called Polygonum multiflorum, has been acknowledged to alleviate Alzheimer's disease (AD)-induced learning disorder in the transgene mice. Because the microglia activation is really important during the AD progression, herein, we determined the effects of TSG on AD neuropathology, microglia polarization and its underlying mechanism. We used APP/PS1 mice along with immunohistochemistry and immunofluorescence techniques to evaluate the function of TSG as 60, 120 and 180 mg/kg on Aβ deposition, neuronal loss and microglia polarization induced by AD. Additionally, we assessed the effects of TSG on TREM2 signalling using both molecular docking and Western blot analysis. TSG was found to promote neuronal survival and decrease Aβ deposition in APP/PS1 mice. Moreover, TSG reduced microglia M1 polarization and modulated the TREM2/PI3K/AKT signalling pathways. TSG could reduce neuronal impairment by mediating the microglia polarization by TREM2/PI3K/AKT signalling pathway in APP/PS1 mice and is a latent pharmacological research direction for the therapy in the patients with AD.

Over the past years, multiple severe oil spills stemmed from oil exploitation have occurred frequently, which has continually endangered the future development of marine life and human beings. Under such circumstance, plastics has gradually become an essential part of the current oil absorption field. Polystyrene foam microspheres are extensively utilized in the domain of oil absorption owing to their significant specific surface area, superb adsorption characteristics, and low density. First and foremost, this review is predominantly intended to summarize various functional modification methods of polystyrene foams applied to oil absorption fields. It is mainly divided into two categories, namely polystyrene as the main body to be modified and polystyrene as an object participating in the modification. Furthermore, this review probes deep into the essential technological parameters that affect the oil absorption rate, which is primarily materialized by electrospinning, high inward emulsion (HIPE) and other modification approaches. Ultimately, this review also explores and reviews the economic feasibility of employing polystyrene matrix to make oil absorption material for oil spill repair. It is expected to provide some design ideas and inspiration for future workers to develop suitable, convenient, high oil absorption polystyrene-based oil-absorbent materials.

ETHNOPHARMACOLOGICAL RELEVANCE:Long-term neurological dysfunction following stroke significantly impairs patients' quality of life. Ginkgo biloba L (GBL), a traditional Chinese herbal medicine, has shown promise in treating ischemic stroke and related disorders. Diterpene Ginkgolides Meglumine Injection (DGMI), derived from GBL, has demonstrated improved recovery outcomes in stroke patients when administered during the hyperacute phase (HAP) in clinical studies, yet the underlying mechanisms remain elusive. MATERIALS AND METHODS:Utilizing a Transient Middle Cerebral Artery Occlusion (tMCAO) model, we evaluated the effects of DGMI at varying doses and administration times on neurological function, brain injury, and identified key genes/pathways via RNA-seq and bioinformatics analyses, validated by RT-PCR. An in vitro LPS-induced astrocyte activation model was used to evaluate DGMI's anti-inflammatory effects. RESULTS:DGMI administered during the hyperacute phase (HAP, 0.5 h post-tMCAO) exhibited superior neuroprotection compared to the acute phase (AP, 24 h post-tMCAO) in mice. HAP-DGMI significantly enhanced survival rates, reduced neurological deficit scores, infarct sizes, and neuronal apoptosis, with more pronounced improvements observed on days 3 and 7 post-tMCAO. Transcriptome sequencing revealed that HAP-DGMI more effectively normalized abnormal gene expression profiles, particularly in genes involved in immune and inflammatory pathways, in both motor (M1) and sensory (S1) cortices. Additionally, HAP-DGMI reversed a higher proportion of disease-characteristic pathways compared to AP. CONCLUSIONS:These findings underscore the potential of early HAP intervention with DGMI in enhancing neuroprotection and functional recovery in AIS bymodulating key immune and inflammatory genes and pathways, providing experimental and theoretical support for the clinical application of DGMI.

The polysaccharides are abundant in nature and are typically considered harmless. They can be chemically modified to exhibit a diverse range of fluorescent behaviors. Moreover, these characteristics render polysaccharides particularly promising future for the development of environmentally friendly materials, such as chemical sensors. In this study, a chitosan-based dual-mode sensor (CS-DAS) with aggregation-induced emission (AIE) properties was designed for both fluorometric and colorimetric detection of nitrite. The unique AIE property of CS-DAS enables enhanced fluorescence in aggregated states, overcoming conventional quenching limitations. CS-DAS also showed high selectivity and sensitivity for nitrite detection. By fluorescence and colorimetry, the limits of detection were calculated to be 0.021 mu M (1.45 mg/kg) and 0.027 mu M (1.86 mg/kg), respectively. This sensor was successfully utilized for the detection of nitrite in sausage samples. Additionally, it exhibited significant antibacterial activity against typical Gram-positive and Gram-negative bacteria. Moreover, CS-DAS showed low cytotoxicity, demonstrating its potential as an excellent fluorescent probe for cell imaging applications.

Polysaccharides, as a natural biomolecule, are abundantly available in nature and have good bioactivity. They contain several functional groups such as hydroxyl, carboxyl, and amino groups, which can exhibit different fluorescent property after modification. In this work, the chitosan (CS) was selected as a raw material and grafted with methotrexate (MTX) to prepare a nitrite sensor. The sensing material exhibited obvious aggregation-induced emission (AIE) properties and could react with nitrite under acidic conditions to form diazo compounds that could enhance fluorescence. This "enhanced-luminescent" mode fluorescence probe for nitrite (NO2-) displayed superior sensing performance, such as excellent sensitivity, good selectivity, a low detection limit (0.22 μM) and wide detection range from 0 to 120 μM. Moreover, this sensor was effectively applied to detect nitrite in sausage samples. Finally, CS-MTX also showed excellent biocompatibility, good water solubility and outstanding antibacterial performance against Gram-positive Staphylococcus aureus (S. aureus) and Gram-negative Escherichia coli (E. coli). These results demonstrated that it may be a potent multifunctional material for nitrite detection and anti-bacteria in food industry.

Metabolic studies at the single cell level can directly define the cellular phenotype closest to physiological or disease states. However, the current single cell metabolome (SCM) study using mass spectroscopy has difficulty giving a complete view of the metabolic activity in the cell, and the prediction of the metabolism-phenotype relationship is limited by the potential inconsistency between transcriptomic and metabolic levels. Here, the single-cell simultaneous metabolome and transcriptome profiling method (scMeT-seq) is developed at one single cell, based on sub-picoliter sampling from the cell for the initial metabolome profiling followed by single cell transcriptome sequencing. This design not only provides sufficient cytoplasm for SCM but also nicely keeps the cellular viability for the accurate transcriptomic analysis in the same cell. Integrative analysis of scMeT-seq reveals both dynamical and cell state-specific associations between metabolome and transcriptome in the macrophages with defined metabolic perturbations. Moreover, metabolite signatures are mapped to the single-cell trajectory and gene correlation network of macrophage transition, which allows the unsupervised functional interpretation of metabolome. Thus, the established scMeT-seq should lead to a new perspective in metabolic research by transforming metabolomics from a metabolite snapshot to a functional approach.

Traditional Chinese medicine has been utilized in China for approximately thousands of years in clinical settings to prevent Alzheimer's disease (AD) and enhance memory, despite the lack of a systematic exploration of its biological underpinnings. Exciting research has corroborated the beneficial effects of tetrahydroxy stilbene glycoside (TSG), an extract derived from Polygonum multiflorum, in delaying learning and memory impairment in a model that mimics AD. Therefore, the primary objective of this study is to investigate the major function of TSG upon protein regulation in AD. Herein, a novel approach, encompassing data independent acquisition (DIA), DIA phosphorylated proteomics, and parallel reaction monitoring (PRM), was utilized to integrate quantitative proteomic data collected from APP/PS1 mouse model exhibiting toxic intracellular aggregation of Aβ. Initially, we deliberated upon both single and multi-dimensional data pertaining to AD model mice. Furthermore, we authenticated disparities in protein phosphorylation quantity and expression, phosphorylation function, and ultimately phosphorylation kinase analysis. In order to validate the results, we utilized PRM ion monitoring technology to identify potential protein or peptide biomarkers. In the mixed samples, targeted detection of 50 target proteins revealed that 26 to 33 target proteins were stably detected by PRM. In summary, our findings provide new candidates for AD biomarker, which have been identified and validated through protein researches conducted on mouse brains. This offers a wealth of potential resources for extensive biomarker validation in neurodegenerative diseases.SignificanceDIA phosphorylated proteomics technique was used to detect and analyze phosphorylated proteins in brain tissues of mice with AD. Data were analyzed by various bioinformatics tools to explore the phosphorylation events and characterize them related to TSG. The results of DIA were further verified by PRM. Besides, we mapped the major metabolite classes emerging from the analyses to key biological pathways implicated in AD to understand the potential roles of the molecules and the interactions in triggering symptom onset and progression of AD. Meanwhile, we clarified that in the context of AD onset and TSG intervention, the changes in proteins, protein phosphorylation, phosphorylation kinases, and the internal connections.