Gentian is a traditional Chinese herb with heat-clearing, damp-drying, inflammation-alleviating and digestion-promoting effects, which is widely used in clinical practice. However, there are many species of gentian. According to the pharmacopoeia, Gentiana manshurica Kitag, Gentiana scabra Bge, Gentiana triflora Pall and Gentianarigescens Franch are included. Therefore, accurately identifying the species of gentian is important in clinical use. In recent years, with the advantages of low cost, convenience, fast analysis and high sensitivity, infrared spectroscopy (IR) has been extensively used in herbal identification. Unlike one-dimensional spectroscopy, a two-dimensional correlation spectrum (2D-COS) can improve the resolution of the spectrum and better highlight the details that are difficult to detect. In addition, the residual neural network (ResNet) is an important breakthrough in convolutional neural networks (CNNs) for significant advantages related to image recognition. Herein, we propose a new method for identifying gentian-related species using 2D-COS combined with ResNet. A total of 173 gentian samples from seven different species are collected in this study. In order to eliminate a large amount of redundant information and improve the efficiency of machine learning, the extracted feature band method was used to optimize the model. Four feature bands were selected from the infrared spectrum, namely 3500–3000 cm⁻¹, 3000–2750 cm⁻¹, 1750–1100 cm⁻¹ and 1100–400 cm⁻¹, respectively. The one-dimensional spectral data were converted into synchronous 2D-COS images, asynchronous 2D-COS images, and integrative 2D-COS images using Matlab (R2022a). The identification strategy for these three 2D-COS images was based on ResNet, which analyzes 2D-COS images based on single feature bands and full bands as well as fused feature bands. According to the results, (1) compared with the other two 2D-COS images, synchronous 2D-COS images are more suitable for the ResNet model, and (2) after extracting a single feature band 1750–1100 cm⁻¹ to optimize ResNet, the model has the best convergence performance, the accuracy of training, test and external validation is 1 and the loss value is only 0.155. In summary, 2D-COS combined with ResNet is an effective and accurate method to identify gentian-related species.

Coxsackievirus B3 (CVB3) is a primary causative agent of viral myocarditis (VMC), which can lead to both acute and chronic cardiac inflammation accompanied by progressive heart failure and arrhythmias. Although CVB3 has been implicated in various forms of programmed cell death, whether it triggers necroptosis and the underlying mechanisms remains unclear. This study aimed to investigate the role and mechanism of CVB3-induced necroptosis and its effect on viral replication. Using both in vitro and in vivo models, we demonstrated that CVB3 infection significantly upregulates the expression of key necroptotic markers RIP1 and RIP3 in HeLa cells and mouse myocardial tissues. This upregulation was accompanied by elevated intracellular reactive oxygen species (ROS) levels and suppression of the Nrf2/HO-1 antioxidant pathway. Intervention with the necroptosis inhibitor Necrostatin-1 (Nec-1) or the ROS scavenger N-acetylcysteine (NAC) markedly attenuated cell death, suppressed viral replication, and ameliorated myocardial injury and inflammatory responses in infected mice. Mechanistically, CVB3 inhibits the Nrf2/HO-1 pathway, thereby inducing substantial ROS accumulation that promotes necroptosis. This effect can be reversed by NAC treatment. Our study reveals a novel mechanism through which CVB3 induces ROS-dependent necroptosis via the suppression of the Nrf2/HO-1 pathway, providing new insights into the pathogenesis of viral myocarditis and suggesting potential therapeutic strategies.

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with unclear pathogenic mechanisms. Dysregulated zinc metabolism contributes to AD pathology. This study aimed to identify zinc metabolism-related hub genes to provide potential biomarkers and therapeutic targets for AD. Methods: We performed an integrative analysis of multiple transcriptomic datasets from AD patients and normal controls. Differentially expressed genes and weighted gene co-expression network analysis (WGCNA) were combined to identify hub genes. We then conducted Gene Set Enrichment Analysis (GSEA), immune cell infiltration analysis (CIBERSORT), and receiver operating characteristic (ROC) curve analysis to assess the hub gene’s biological function, immune context, and diagnostic performance. Drug-gene interactions were predicted using the DrugBank database. Results: We identified a single key zinc transporter–related hub gene, SLC30A3, which was significantly downregulated in AD and demonstrated potential diagnostic value (AUC 0.70–0.80). Lower SLC30A3 expression was strongly associated with impaired synaptic plasticity (long-term potentiation, long-term depression, calcium signaling pathway, and axon guidance), mitochondrial dysfunction (the citrate cycle and oxidative phosphorylation), and pathways common to major neurodegenerative diseases (Parkinson’s disease, AD, Huntington’s disease, and amyotrophic lateral sclerosis). Furthermore, SLC30A3 expression correlated with specific immune infiltrates, particularly the microglia-related chemokine CX3CL1. Zinc chloride and zinc sulfate were identified as potential pharmacological modulators. Conclusions: Our study systematically identifies SLC30A3 as a novel biomarker in AD, linking zinc dyshomeostasis to synaptic failure, metabolic impairment, and neuroimmune dysregulation. These findings offer a new basis for developing targeted diagnostic and therapeutic strategies for AD.

Viral myocarditis (VMC), predominantly driven by Coxsackievirus B3 (CVB3) infection and the resultant excessive immune response, lacks effective treatments and specific antiviral drugs in clinical practice. Chlorogenic acid (CGA) has been proven to have significant antiviral and anti-inflammatory properties. This study evaluated the potential and mechanism of action of CGA against CVB3-induced viral myocarditis. Our research results showed that CGA significantly alleviated myocardial tissue damage in vivo. This protective effect was accompanied by effective inhibition of myocardial inflammatory responses and viral replication. Further in vitro experiments confirmed that CGA significantly inhibited the replication of CVB3 in a dose-dependent manner, and its inhibitory effect mainly targeted the replication stage of the viral life cycle. Mechanistically, CGA treatment correlates with reduced ZBP1 expression and accelerated ZBP1 degradation involving the ubiquitin–proteasome pathway, accompanied by suppressed activation of PANoptosis markers. These findings suggest that CGA alleviates CVB3-induced myocarditis through concerted antiviral and anti-inflammatory effects, with ZBP1-mediated PANoptosis as a potential contributing mechanism.

Wound healing is frequently compromised by excessive oxidative stress, prolonged inflammation, and inadequate tissue regenerative capacity. To address these challenges, a thermosensitive and injectable composite hydrogel based on Pluronic F127 (F127), phosphatidylcholine (PC), and L-lysine (Lys) was developed for the sustained delivery of sinomenine–gallic acid nanoparticles (SGNPs) and the acceleration of wound repair. The hydrogel undergoes a rapid sol–gel transition at physiological temperatures through physical interactions, enabling excellent injectability and in situ gelation. The optimized composite hydrogel exhibited improved mechanical properties, enhanced structural stability, and a uniform porous microarchitecture. The F127−Lys−PCF127−Lys−PC@SGNPs hydrogel showed superior overall stability and hemocompatibility while enabling the sustained release of SGNPs for up to 24 h. Benefiting from the incorporation of SGNPs, the composite hydrogel displayed enhanced antioxidant activity, effectively scavenging free radicals and alleviating cellular oxidative stress. In vitro experiments demonstrated that the hydrogel promoted keratinocyte migration and proliferation. Furthermore, in a murine full-thickness skin wound model, treatment with F127−Lys−PCF127−Lys−PC@SGNPs significantly accelerated wound closure and facilitated re-epithelialization, angiogenesis, and collagen deposition. Collectively, this multifunctional thermosensitive hydrogel provides a promising platform for advanced wound dressings that integrate sustained delivery, antioxidant protection, and tissue regeneration.

Venous thromboembolism (VTE) is a major cause of morbidity and mortality, underscoring the need for new molecular markers to enable early detection and clarify underlying mechanisms. Iron metabolism is linked to oxidative stress, endothelial injury, and inflammation, all central to thrombosis, yet its transcriptomic contribution to VTE remains unclear. We analyzed gene expression profiles from GSE19151 and GSE48000 using differential expression and weighted gene co-expression network analysis (WGCNA), integrating results with an iron metabolism gene set. Three hub genes were identified, arachidonate 5-lipoxygenase (ALOX5), Rho GTPase activating protein 1 (ARHGAP1), and glucose-6-phosphate dehydrogenase (G6PD), all downregulated in VTE. Gene set enrichment indicated that ALOX5 is involved in endothelial regulation, lipid metabolism, and immune pathways. A three-gene signature showed high diagnostic accuracy (AUC = 0.924 in the discovery cohort; 0.705 in validation). Immune deconvolution revealed broad immune remodeling and associated ALOX5 with multiple immune cell subsets, especially M0 macrophages, and with regulators such as TGFB1 and IL6R. Western blot analysis further showed that ALOX5 protein expression was significantly increased in LPS-activated HUVECs, supporting its involvement in inflammatory endothelial injury. DrugBank screening identified 19 approved drugs targeting ALOX5, supporting its potential for mechanistic and clinical investigation.