EXCLI Journal最新文献

This review delves into the antimicrobial potential of essential oils (EOs), focusing on their mechanisms of action against foodborne pathogens and their applications as natural food preservatives. EOs, derived from aromatic plants, are complex mixtures of volatile compounds, primarily terpenes, terpenoids, and phenolic compounds, which exhibit potent antimicrobial properties. These bioactive compounds disrupt bacterial cell membranes, increase permeability, and induce leakage of intracellular components, leading to cell death. Additionally, EOs inhibit energy production by depleting ATP levels, disrupting the tricarboxylic acid cycle, and impairing cellular respiration. They also generate reactive oxygen species (ROS), causing oxidative stress and damaging bacterial DNA, proteins, and lipids. Furthermore, EOs interfere with quorum sensing and biofilm formation, reducing bacterial virulence and resistance. Despite their efficacy, challenges such as strong flavors, poor solubility, and environmental sensitivity limit their direct application. To address these issues, encapsulation techniques, such as nanoemulsions and active packaging, have been developed to enhance the stability and controlled release of EOs. For instance, nanoencapsulation of thyme and cinnamon EOs has significantly improved their antimicrobial efficacy in food products like milk and minced meat. By harnessing the multifaceted mechanisms of EOs, this review underscores their potential as sustainable and effective natural preservatives to combat foodborne pathogens and improve food safety. See also the graphical abstract(Fig. 1).

Cadmium can surpass fetal circulation and the blood-brain barrier due to its similar physicochemical properties to those of other divalent metals and causes diverse neuronal disorders. Previous reports have suggested a possible link between epigenetic alterations and neuronal changes in offspring due to cadmium exposure at different developmental stages. Hypermethylation of the glucocorticoid receptor NR3C1 disturbs the development of the hypothalamic-pituitary-adrenal axis, which in turn is responsible for the abnormal cognitive behavior of neonates. In addition, the upregulation of placental miR-509-3p and miR-193-5p expression was found to be the major cause of impaired development of the central nervous system. In this review, the epigenetic mechanism of cadmium-mediated neurotoxicity is described. Moreover, the journey of cadmium from the maternal body to the fetal body through circulation and to the neonatal body through breast milk is also tracked. The vulnerability of developing fetuses to cadmium is an alarming issue. Different types of epigenetic changes, such as DNA methylation, altered miRNA expression and histone modifications, are induced by cadmium and lead to various types of neurodevelopmental disorders. We hope this narrative review will provide distinct knowledge of the transportation of cadmium and its adverse effects on fetal neurodevelopment. See also the graphical abstract(Fig. 1).

Bupleurum falcatum L. is known for its therapeutic properties, especially in treating fever, inflammation, and infectious diseases. However, its potential for dermatological applications remains mainly unexplored. Thus, the present study explores antimicrobial potential of B. falcatum against biofilm-associated infections, antibiotic-resistant strains, and UV-induced skin damage. This aligns with the growing interest in natural products as sources of bioactive compounds with skin-protecting features. Herein, we employed maceration (M) and ultrasound-assisted extraction (USA) at 50 Hz and 100 Hz (USA 50 and USA 100) to obtain extracts from aerial parts of the plant. Chemical profiling was performed using UHPLC. Antimicrobial activity, biofilm inhibition, EPS and eDNA production were assessed using microdilution test, crystal violet, Congo red, and eDNA assays, respectively. Cytotoxicity and photoprotective effects were evaluated on human keratinocytes using the MTT assay. Chemical analysis identified 64 compounds, including benzoic and cinnamic acid derivatives, flavonoid glycosides, and saikosaponins. Extracts showed strong antimicrobial activity against Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MIC as low as 0.5 mg/mL). The M extract displayed moderate biofilm inhibition and reduced eDNA production. Cytotoxicity assays confirmed safety on keratinocytes, while M and USA 100 extracts demonstrated photoprotective effects. B. falcatum extracts showed promising potential in addressing biofilm-associated infections, antibiotic resistance, and UV-induced skin damage. See also the graphical abstract(Fig. 1).

This immunoinformatics-based study utilized a suite of online predictive tools to characterize the structural and immunogenic properties of Toxoplasma gondii rhoptry neck proteins (TgRONs). Full-length amino acid sequences of TgRON2, TgRON4, TgRON4L1, TgRON5, TgRON8, TgRON9, TgRON10, and TgRON13 were retrieved from ToxoDB and subjected to comprehensive analysis. Except for TgRON4L1, all proteins were predicted to be possess antigenic potential, with none identified as allergenic. Solubility predictions indicated that TgRON9 and TgRON10 are the most likely to be expressed as soluble antigens. Aliphatic index values, ranging from 51.17 to 84.63, suggest acceptable thermostability, while negative GRAVY scores across all proteins indicate favorable hydrophilicity. Additionally, multiple post-translational modification sites were identified, underscoring the functional complexity of these antigens. Initial 3D structure modeling showed that 60.21-92.41 % of residues fell within favored regions on Ramachandran plots, with refinement increasing this to 92.27-98.58 %, reflecting substantial improvements in structural quality. Several potential T-cell (CTL and HTL) and B-cell epitopes were predicted for all candidate proteins. Immune simulation models further suggested that these antigens could elicit robust humoral and cellular immune responses when delivered in a three-dose regimen at four-week intervals. These findings offer valuable preliminary insights and support the further investigation of TgRONs, particularly TgRON9 and TgRON10, as promising targets for experimental validation in the development of vaccines against T. gondii infection. See also the graphical abstract(Fig. 1).

Artificial intelligence (AI) and machine learning (ML) are transforming medication discovery, particularly in neuropsychiatric illnesses, where traditional drug research presents major obstacles. This paper looks at how artificial intelligence might help advance neuropsychiatric medication development, with an emphasis on early-stage research, drug design, and clinical diagnostics. This review discusses AI's contribution to understanding the blood-brain barrier and its link with the central nervous system, which is an important aspect of medication efficacy in neuropsychiatric treatments. AI-facilitated de novo drug design, using predictive algorithms and deep learning models, speeds up the discovery of new medicinal molecules. AI is employed in brain imaging and diagnosis, boosting the accuracy with which neuropsychiatric diseases are identified. BBB permeability prediction is one of the most important uses of AI in drug discovery, as it improves the selection of CNS-active drugs. Additionally, AI is transforming treatment techniques for neurodevelopmental disorders and assisting in the discovery of novel antidepressant medications through data-driven methodologies. Despite these accomplishments, AI-driven drug discovery still has several constraints, such as data biases, regulatory barriers, and ethical issues. Overcoming these restrictions will be critical to unlocking AI's full potential in neuropsychiatric research. This paper concludes with several future possibilities and opportunities, such as incorporating AI into personalized medicine using sophisticated neural network models and multimodal data fusion techniques. This might increase treatment choices for certain conditions by fine-tuning AI approaches. This paper presents a perspective on AI as a highly transformative instrument for influencing neuropsychiatric drug development, as well as an emerging field that has the potential to impact the modern idea of pharmacology. See also the graphical abstract(Fig. 1).

Emerging evidence suggests a strong association between aluminum (Al) exposure and the development of Alzheimer's disease (AD). Due to their nanoscale size and increased surface area, Al nanoparticles (ALNP) exhibit greater neurotoxicity than bulk Al, raising concerns about their role in neurodegenerative disorders. While quercetin has been recognized for its neuroprotective effects, its ability to counteract ALNP-induced hippocampal neurodegeneration and dysregulated MAPK signaling remains largely unexplored. This study investigated the potential of quercetin to ameliorate ALNP-induced memory deficits, alterations in hippocampal stereological parameters, and disruptions in caspase-3 and MAPK signaling in male Swiss mice. Mice (SWR/J, aged 8-10 weeks) received ALNP (10 mg/kg, intraperitoneally for 10 days) with or without quercetin at doses of 1, 10, or 100 mg/kg (orally). Memory performance was assessed using the elevated plus maze (EPM), novel object recognition (NOR), and Y-maze tasks, followed by stereological and western blot analyses of the hippocampus. Our findings revealed that quercetin (100 mg/kg) significantly preserved hippocampal volume and neuronal integrity in the dentate gyrus (DG) and Cornu Ammonis 1 (CA1)-key regions involved in memory processing and output signaling. Additionally, quercetin modulated MAPK signaling by enhancing ERK phosphorylation while suppressing ALNP-induced activation of p38 and cleaved caspase-3, suggesting a role in reducing neuroinflammation and apoptosis. This is the first study to demonstrate that quercetin can counteract the neurotoxic effects of ALNP, highlighting its potential as a therapeutic strategy against nanoparticle-induced neurodegeneration in an Alzheimer's-like model. See also the graphical abstract.(Fig. 1).