Sleep and immunity interact through a highly coordinated “sleep-immune axis” to maintain physiological homeostasis. Sleep optimizes immune cell trafficking through neuroendocrine pathways, suppresses sympathetic nervous activity to mitigate inflammation, and regulates microglial polarization to sustain neuroimmune balance. In return, immune signals shape sleep architecture: pro-inflammatory cytokines activate thalamic neurons to enhance slow-wave sleep (SWS), microglia inhibit norepinephrine release via the P2Y12-Gi-Ca²⁺ pathway, and peripheral immune activation feeds back to regulate sleep-wake cycles. Dysregulation of this bidirectional axis constitutes a pathogenic link to cardiovascular diseases, neurodegenerative disorders, autoimmune diseases, and metabolic disorders. Sleep loss reprograms immune phenotypes, amplifies systemic inflammation, and compromises immune surveillance, whereas immune dysregulation, such as TREM2 deficiency or autoimmune injury to orexinergic neurons, directly impairs sleep regulation. Therapeutic interventions targeting key nodes, including STING pathway activation, adenosine-modulating light therapy, and gut microbiota modulation, hold promise for restoring sleep–immune homeostasis and improving outcomes in comorbid disease states.

Background: Oral cancer is a significant global health concern, often diagnosed at advanced stages with poor prognosis and high mortality rates. Early detection of malignant and premalignant oral lesions is crucial for improving patient outcomes. This observational study aims to identify specific regions of oral lesions for histopathological diagnosis and assess the correlation between toluidine blue dye uptake in oral tissues and histopathological findings in premalignant and cancerous lesions. Methods: A total of 216 cases of oral lesions were selected based on predetermined inclusion and exclusion criteria without restrictions on age, gender, religion, or socioeconomic status. Patients were identified through medical records and clinical investigations, focusing on individuals with nonhealing oral ulcers persisting for over three weeks without a prior clinical diagnosis of oral cancer. Only toluidine blue-positive cases were considered for further examination. Histopathological analyses were performed on toluidine blue-positive areas to determine the presence of premalignant and malignant lesions. Results: Among the 216 cases, histopathological findings revealed 98 cases of hyperplastic epithelium, 14 cases of verrucous carcinoma, 34 cases of premalignant lesions, 12 cases of dysplasia, and 58 cases of squamous cell carcinoma (SCC). The toluidine blue dye demonstrated a 100% staining response rate, with an 86.2% accuracy in detecting carcinoma and a 15.7% accuracy for premalignant lesions. A significant histopathological difference was observed between oral potentially malignant lesions and SCC. Conclusion: The findings indicate that toluidine blue dye can enhance the early detection of malignant and premalignant oral lesions, improving diagnostic accuracy compared to traditional visual or therapeutic approaches. This method can aid clinicians in identifying high-risk oral lesions promptly, potentially improving patient outcomes.

Background: Liver cancer is a major cause of cancer-related mortality worldwide, and effective therapeutic strategies remain limited. Salidroside, a bioactive compound derived from Rhodiola rosea, has demonstrated anti-inflammatory and anticancer properties; however, its molecular mechanisms in liver cancer remain unclear. Methods: Keywords for “liver,” “liver cancer,” and “salidroside” were identified using the PubMed MeSH database. Protein-coding target genes were retrieved from the GeneCards, Traditional Chinese Medicine Systems Pharmacology (TCMSP), UniProt, HERB, and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Intersection genes were identified using Venn analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed in Metascape (Homo sapiens, p < 0.05). Protein-protein interaction (PPI) networks were constructed via STRING and analyzed with Cytoscape using the Maximal Clique Centrality algorithm to identify hub genes. Finally, an integrative “liver-liver cancer-salidroside-target-signaling pathway” network was generated to visualize potential mechanisms. Results: Venn analysis identified 73 intersection genes among liver, liver cancer, and salidroside targets. GO enrichment revealed roles in cellular stress response, apoptosis regulation, and mitochondrial function, while KEGG analysis highlighted pathways including PI3K-Akt signaling, apoptosis, and cancer-related pathways. PPI analysis identified key hub genes, including KT Serine/Threonine Kinase 1 (AKT1), Hypoxia-Inducible Factor 1-Alpha (HIF1A), and B-cell lymphoma 2 (BCL2), etc. The integrated network elucidated potential interactions between salidroside, target genes, and enriched pathways. Conclusions: Salidroside may exert anti-liver cancer effects by modulating apoptosis, oxidative stress, and cancer signaling pathways via hub genes like AKT1 and HIF1A. This study provides novel insights into salidroside’s therapeutic potential, warranting further experimental validation.

Background: Rectal cancer is a major global health challenge, and the pharmacological mechanisms of natural compounds for its treatment remain unclear. Gastrodin, a bioactive component from Gastrodia elata, has shown anticancer potential, but its molecular targets in rectal cancer are largely unknown. This study aimed to systematically explore the key targets and signaling pathways of Gastrodin against rectal cancer using network pharmacology. Methods: Targets related to the rectum, rectal cancer, and Gastrodin were collected from GeneCards, Traditional Chinese Medicine Systems Pharmacology (TCMSP), and other databases. Overlapping genes were identified through Venn analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed, followed by the construction of protein-protein interaction (PPI) networks using STRING database and the identification of hub genes with the MCC algorithm in Cytoscape. A comprehensive regulatory network linking Gastrodin, intersecting genes, and KEGG pathways was visualized in Cytoscape. Results: Fifteen overlapping targets were identified, enriched in biological processes related to apoptosis regulation, immune activation, and the MAPK cascade. KEGG analysis highlighted ten significantly enriched pathways (adjusted p < 0.05), with cytosolic DNA-sensing, alcoholic liver disease, and insulin resistance pathways being the most prominent, suggesting a role in immune modulation and inflammation. PPI network analysis pinpointed IL6, IL1B, and NFKB1 as key hub genes. The integrated network revealed that Gastrodin may exert multi-target effects by regulating immune and apoptotic signaling cascades. Conclusion: This study systematically elucidates the multi-target and multi-pathway mechanisms of Gastrodin against rectal cancer, emphasizing its roles in immune modulation and apoptosis regulation. These findings provide a theoretical basis for further experimental validation of Gastrodin as a potential adjunctive therapeutic candidate.

Background: Multiple organ dysfunction syndrome (MODS) is often accompanied by severe liver injury, yet effective therapeutic options remain limited. Salidroside (SAL), a natural compound derived from Rhodiola rosea, has shown protective effects in various pathological conditions. This study aimed to elucidate the potential molecular mechanisms of SAL in MODS-associated liver injury through a network pharmacology approach. Methods: Potential targets of MODS, liver, and SAL were obtained from the GeneCards database, and overlapping targets were identified by Venn analysis. A protein–protein interaction (PPI) network was constructed using the STRING database, and hub targets were screened by topological analysis. Functional annotation was performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. An integrated “Disease-Site-Drug-Key Target-KEGG Pathway” network was then established to visualize the potential therapeutic mechanisms. Results: Six intersecting targets were identified, forming a PPI network with 15 interactions. GO enrichment indicated involvement in transcriptional regulation, inflammatory response, apoptosis, and autophagy. KEGG analysis revealed 57 significantly enriched pathways, particularly those related to immune checkpoints, hypoxia-inducible factor 1 (HIF-1) signaling, cancer-associated pathways, lipid metabolism, infectious diseases, and neurodegeneration. The integrative network highlighted the association between SAL, key targets, and multiple signaling pathways relevant to MODS-associated liver injury. Conclusion: This study suggests that SAL may exert protective effects on MODS-related liver injury by modulating inflammation, apoptosis, metabolism, and immune responses. These findings provide a theoretical basis for further experimental validation and potential clinical application of SAL in MODS therapy.

Background: Rectal cancer is a significant health concern, and Panax notoginseng saponins (PNS), a traditional Chinese medicine component, shows potential therapeutic effects. This study aimed to identify key gene targets and underlying mechanisms of PNS in rectal cancer using bioinformatics approaches. Methods: Standardized keywords were used to retrieve gene targets from the GeneCards and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Venn analysis was applied to identify overlapping genes among rectum, rectal cancer, and PNS. Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using the Metascape and Weshengxin platforms. Protein–protein interaction (PPI) networks were constructed via STRING and visualized with Cytoscape to identify hub genes and regulatory interactions. Results: A total of 1,388 rectal cancer-related, 2,889 rectum-related, and 37 PNS-related gene targets were identified. Venn analysis revealed 20 overlapping genes. GO enrichment analysis indicated that these genes were primarily involved in biological processes such as cell migration, localized to cellular components including protease inhibitor complexes, and exhibited molecular functions such as cytokine receptor binding. KEGG pathway analysis highlighted key signaling pathways like AGE-RAGE signaling pathway in diabetic complications. PPI network analysis identified 10 hub genes, such as interleukin-6 (IL6), tumor necrosis factor (TNF), AKT Serine/Threonine Kinase 1 (AKT1). The regulatory network was constructed by revealing critical interactions among rectum, rectal cancer, PNS, hub genes, and associated pathways. Conclusion: This study systematically elucidates the potential molecular mechanisms of PNS in rectal cancer, identifying key gene targets and signaling pathways, providing a foundation for future mechanistic and therapeutic research.

Background: Lung cancer (LC) remains the leading cause of cancer-related mortality worldwide, underscoring the urgent need for more effective therapeutic strategies. Notoginsenoside R1 (NGR1), a major bioactive component derived from Panax notoginseng, exhibits diverse pharmacological properties. However, its molecular mechanisms against LC have not been fully elucidated. This study employed a network pharmacology approach to investigate the potential anti-LC mechanisms of NGR1. Methods: Relevant targets of NGR1 and LC were identified using precise PubMed MeSH terms and data mining from GeneCards, the Traditional Chinese Medicine Systems Pharmacology (TCMSP), HERB, and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Shared targets were determined through Venn diagram analysis. A protein-protein interaction (PPI) network was constructed using the STRING database and visualized with Cytoscape. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to explore the associated biological functions and signaling pathways. Results: A total of 36 intersecting genes were identified as common targets of NGR1 and LC. The PPI network revealed key interactions among these targets, from which 10 hub genes were identified. GO analysis indicated that these targets were mainly involved in the establishment or maintenance of transmembrane electrochemical gradients, phosphatidylinositol 3-kinase complex (class IA), and steroid hormone binding. KEGG analysis showed significant enrichment in the AGE-RAGE signaling pathway involved in diabetic complications, suggesting its relevance to LC progression. Conclusions: This study highlights the multi-target and multi-pathway characteristics of NGR1 in LC treatment, offering a theoretical foundation for future drug development.

Breast cancer remains the most prevalent malignancy and a major therapeutic challenge in women worldwide, with the tumor immune microenvironment (TIME) playing a pivotal role in disease progression and treatment resistance. Tumor-derived extracellular vesicles (TEVs) serve as critical mediators of intercellular communication within TIME by transporting bioactive molecules such as proteins, nucleic acids, and lipids, thereby modulating both innate and adaptive immune responses to promote immunosuppression and immune evasion. TEVs deliver immunosuppressive factors, including programmed death-ligand 1 (PD-L1), transforming growth factor-beta (TGF-β), and specific miRNAs, which impair dendritic cell maturation, drive macrophage polarization toward an M2-like phenotype, suppress nature killer (NK) cell cytotoxicity, and induce T-cell exhaustion or regulatory T-cell expansion. Beyond their immunosuppressive roles, TEVs hold significant diagnostic and prognostic potential, functioning as non-invasive biomarkers (e.g., human epidermal growth factor receptor 2 (HER2), epithelial cell adhesion molecule (EpCAM), and miR-21 detection) and predictors of immunotherapy response. Therapeutic strategies targeting TEV biogenesis, release, or cargo may enhance immunotherapy efficacy, while engineered TEVs loaded with tumor antigens or immunostimulatory molecules, offer novel immunotherapeutic opportunities. However, challenges such as TEV heterogeneity, standardization in isolation techniques, in vivo targeting efficiency, and safety concerns hinder clinical translation. Future research should integrate multidisciplinary approaches to optimize TEV-based applications, advancing their potential as diagnostic tools and personalized immunomodulatory therapies in breast cancer.

Lung cancer remains one of the most prevalent and deadly malignancies worldwide, posing a significant threat to public health. While conventional treatments such as surgery, chemotherapy, and radiotherapy can suppress tumor progression to some extent, they are often accompanied by severe side effects and limited long-term efficacy. In recent years, advances in medical technology have led to the emergence of immunotherapy as a promising alternative approach. However, there is a lack of comprehensive reviews that summarize and integrate the latest developments in this field. This study provides an overview of recent progress in lung cancer immunotherapy by analyzing 200 publications retrieved from the PubMed database, of which 133 were systematically reviewed. The review covers the immunological landscape of lung cancer, including its epidemiology, current treatment strategies, anti-tumor immune mechanisms, and the application of immune checkpoint inhibitors and other immunotherapeutic modalities. By highlighting key advances and emerging trends over the past decade, this review aims to offer valuable insights for clinicians and researchers, contributing to the ongoing improvement of lung cancer management and therapeutic outcomes.

The incidence rate of diabetes is increasing year by year, and the role of intestinal microbiota in this process has garnered considerable attention. In type 1 diabetes, the imbalance of intestinal microbiota can lead to disease by disrupting the intestinal barrier, altering immune regulation, and changing metabolites and specific microbial abundance, all of which are influenced by age, genetics, environment, and other factors. The corresponding treatment strategies include prebiotics, probiotics, traditional Chinese medicine (TCM), and fecal microbiota transplantation, but still need to be optimized. Changes in intestinal microbiota composition and metabolites in patients with type 2 diabetes affect related signaling pathways. Besides, diet and drugs also affect intestinal microbiota and diseases. In terms of complications associated with diabetes, intestinal microbiota is closely linked to diabetic encephalopathy, nephropathy, retinopathy, neuropathy, and cardiomyopathy. It participates in the pathological process by regulating metabolism, influencing inflammatory reactions, and other mechanisms. Treatment strategies based on intestinal microbiota have potential in treating these complications, but face many challenges. This review focuses on the research progress of intestinal microbiota, diabetes, and its complications. In the future, in-depth exploration of molecular mechanisms and large-scale clinical research are still needed.