The prevention, treatment, and rehabilitation of spinal cord injury (SCI) have always posed significant medical challenges. After mechanical injury, disturbances in microcirculation, edema formation, and the generation of free radicals lead to additional damage, impeding effective repair processes and potentially exacerbating further dysfunction. In this context, inflammatory responses, especially the activation of macrophages, play a pivotal role. Different phenotypes of macrophages have distinct effects on inflammation. Activation of classical macrophage cells (M1) promotes inflammation, while activation of alternative macrophage cells (M2) inhibits inflammation. The polarization of macrophages is crucial for disease healing. A non-coding RNA, known as microRNA (miRNA), governs the polarization of macrophages, thereby reducing inflammation following SCI and facilitating functional recovery. This study elucidates the inflammatory response to SCI, focusing on the infiltration of immune cells, specifically macrophages. It examines their phenotype and provides an explanation of their polarization mechanisms. Finally, this paper introduces several well-known miRNAs that contribute to macrophage polarization following SCI, including miR-155, miR-130a, and miR-27 for M1 polarization, as well as miR-22, miR-146a, miR-21, miR-124, miR-223, miR-93, miR-132, and miR-34a for M2 polarization. The emphasis is placed on their potential therapeutic role in SCI by modulating macrophage polarization, as well as the present developments and obstacles of miRNA clinical therapy.

Spinal cord injury (SCI) results in severe neurological deficits due to disrupted neural pathways. While the spinal cord possesses limited self-repair capabilities, recent advancements in hydrogel-based therapies have shown promise. Polyphenol-based hydrogels, known for their neuroprotective properties, offer a suitable microenvironment for neural regeneration. In this study, a novel poly(lipoic acid)/poly(dopamine) adhesive hydrogel was developed as a versatile platform for delivering therapeutic agents. This hydrogel was loaded with methylcobalamin, a neurotrophic factor, and tellurium nanoenzymes, potent antioxidants. The nanoenzymes effectively mitigated oxidative stress and inflammation, while methylcobalamin promoted nerve regeneration. The combined therapeutic effects of the nanoenzymatic hydrogel demonstrated significant efficacy in repairing spinal cord injuries, highlighting its potential as a promising strategy for treating this debilitating condition.

Background: Stem cell transplantation therapy is a potential approach for the repair of spinal cord injuries and other neurodegenerative diseases, but its effectiveness is hampered by the low rate of targeted migration of cells to the area of injury. The aim of this study was to investigate the effects of miR-31 on the migration of bone marrow mesenchymal stem cells (BMSCs) and the regulation of MMP-2 and CXCR4 expression in vitro and in vivo. Methods: eGFP-expressing BMSCs were isolated and cultured for subsequent experiments. The experiments were divided into three groups: control group, miR-31agomir group, and miR-31antagomir group. Proliferation was analyzed using CCK-8 and flow cytometry; cell migration in vitro was analyzed using wound-healing and transwell assays. The mouse SCI model was prepared by the impact method, and cells were transplanted (3 groups, 12 per group). Relevant inflammatory factors were detected by ELISA. The BMS score was used to evaluate the functional recovery of the mouse spinal cord and the frozen section was used to analyze the cell migration ability in vivo. The in vitro and in vivo expression levels of MMP-2 and CXCR4 were evaluated by Western blot and immunohistochemical staining. Results: In vitro experiments showed that cells in the miR-31agomir group exhibited enhanced cell proliferation (P<0.05, P<0.001) and migration (P<0.001) and upregulated protein expression levels of CXCR4 (P<0.01) and MMP-2 (P<0.001) compared with cells in the control group. The results of in vivo experiments showed that the expression of pro-inflammatory factors was reduced after cell transplantation treatment. Cells in the miR-31agomir group showed enhanced cell-targeted migration ability (P<0.001), improved the function of damaged tissues (P<0.001), and upregulated CXCR4 and MMP-2 expression compared to the control group (P<0.001). Conclusion: Our experiment demonstrated that miR-31 could promote the migration of BMSCs and miR-31 could repair and improve the function of damaged tissues in SCI.

Background: Reducing antibiotic dependence in poultry production is critical to mitigating antimicrobial resistance (AMR). Selective breeding for stronger innate immunity may provide a sustainable alternative under a One Health framework. This study investigates whether enhancing monocyte/macrophage phagocytic capacity in layer chickens could improve disease resistance without compromising production performance under antibiotic-free conditions. Methods: Phagocytic capacity was assessed using multiple assays. Phagocytosis product (PP) was measured using the MTT-HCT-8 method, pHrodo-labeled E. coli , and FITC-labeled S. pullorum , whereas the phagocytic index (PI) was determined using O. aries erythrocytes. Chickens were divergently selected into high (HPPG) and low (LPPG) phagocytosis product groups based on monocyte/macrophage phagocytic capacity at 16 weeks of age (wk). Production traits, immune-related gene expression, oxidative stress-related markers, and pathogen-clearance ability were compared between groups using Student's t -test. Results: PP measured by the MTT-HCT-8 method was significantly correlated with PP or PI using the other methods ( P < 0.05, R ² > 0.70). HPPG hens showed significantly higher laying rates at 40 and 60 weeks and greater hatch weight than LPPG hens ( P < 0.05), whereas fertility, hatchability, or semen quality did not differ between groups. HPPG birds exhibited higher interferon-gamma receptor (IFNGR) and Toll-like receptor 2 (TLR2) expression and, after S. pullorum challenge, showed reduced tumor necrosis factor α (TNF-α) and increased microtubule-associated protein 1 light chain 3 alpha (LC3A) expression ( P < 0.05), indicating enhanced pathogen clearance and autophagy without exacerbating oxidative stress or inflammation. Conclusion: Selecting for proper high phagocytic capacity (with a preliminary estimated PP range of 1.58–2.74) improves resistance in layer chickens reared antibiotic-free without reducing productivity and exacerbating oxidative stress or inflammation. These findings support phagocytosis-based phenotyping as a potential balanced-breeding strategy consistent with One Health goals for sustainable poultry production.

Gastrodin, a bioactive ingredient extracted from the Chinese herb Gastrodia gastrodia, has shown potential therapeutic effects in cardiovascular diseases, but its specific role in myocardial infarction is unclear. This study investigated the protective effect of gastrodin on myocardial infarction and its potential mechanism. By clamping the left coronary artery, we created a model of myocardial infarction in C57BL/6J mice. For 14 days, mice in the control and myocardial infarction groups received a daily dose of 100 mg/kg gastrodin. Gastrodin significantly improved cardiac dysfunction in mice with myocardial infarction, decreased heart weight/body weight (HW/BW) and heart weight/tibial length (HW/TL) ratios, and inhibited mRNA expression levels of cardiac fibrosis biomarkers (Collagen Type I (Col1), Collagen Type III (Col3), Matrix Metalloproteinase-2 (MMP-2), Matrix Metalloproteinase-9 (MMP-9)). In addition, gastrodin also inhibited the activity of apoptosis marker Caspase 3, decreased the Bax/Bcl2 mRNA ratio, decreased the expression of pro-inflammatory factors (Interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6)) and pro-inflammatory adhesion molecule Monocyte Chemoattractant Protein-1 (MCP1), and promoted the expression of angiogenesis marker Cluster of Differentiation 31 (CD31). RNA sequencing and Rt-qPCR analysis showed that gastrodin treatment significantly up-regulated the expression of genes related to cell proliferation (Cyclin-Dependent Kinase 1 (CDK1), Threonine Tyrosine Kinase (TTK), Cyclin B2 (CCNB2), Polo-Like Kinase 1 (PLK1)), and promoted the proliferation of human aortic endothelial cells (HAECs). These findings suggest that gastrodin can effectively reduce the pathological changes of myocardial infarction by inhibiting inflammation, reducing apoptosis, and promoting endothelial cell proliferation, thus providing a new strategy for the prevention and treatment of myocardial infarction.