Ionizing radiation (IR) exerts complex, dose-dependent biphasic effects on the central nervous system (CNS). This review systematically elucidates the mechanisms underlying the impact of high- and low-dose radiation on neurocognitive function. High-dose radiation (HDR) triggers severe DNA damage, oxidative stress, and neuroinflammatory cascades, leading to neuronal dysfunction, suppression of neurogenesis, and failure of neural circuit reorganization, ultimately resulting in persistent cognitive decline. In contrast, low-dose radiation (LDR) exhibits a unique dual nature: within certain thresholds, it can activate endogenous protective pathways—including DNA repair and antioxidant defenses—thereby promoting neural plasticity and network homeostasis and demonstrating adaptive responses and neuroprotective potential. The research paradigm is shifting from the traditional linear no-threshold (LNT) model towards a dynamic homeostasis model. Future research should prioritize the development of neuroprotective strategies during radiotherapy for high-dose exposure, optimize irradiation modalities, and develop novel radioprotective agents to improve patient outcomes. For LDR, it is crucial to delineate its biological effects and explore its potential for intervening in neurodegenerative diseases. This review aims to provide an integrated theoretical framework for understanding the dose-dependent biphasic regulation of radiation on neurocognition and to outline future directions for developing related protective and therapeutic strategies.

The aqueous extract of Diaphragma Juglandis Fructus (AED), a by-product of Juglans regia L., represents a promising food-derived functional ingredient with potential benefits for intestinal health. This study evaluated the anti-colitis effects of AED and explored its underlying mechanisms using LPS-stimulated RAW264.7 macrophages and a DSS-induced colitis mouse model. In DSS-induced colitis in mice, AED at 10 μg/mL suppressed pro-inflammatory cytokine production and inhibited JAK1/STAT3 signaling. In DSS-induced colitis in mice, AED at 600 mg/kg for 7 days mitigated DSS-induced colonic injury, restored tight junction proteins, and improved epithelial barrier integrity. Integrated transcriptomic and metabolomic analyses identified AED-associated alterations in arginine-polyamine and taurine-hypotaurine metabolism, while network pharmacology and molecular docking suggested angiotensin-converting enzyme (ACE) and von Willebrand factor (VWF) as candidate functional targets for further investigation. Collectively, these findings indicate that AED exerts anti-colitis effects in association with coordinated changes in inflammatory signaling, metabolic pathways, and barrier-related markers, supporting its potential as a food-derived functional ingredient candidate for ulcerative colitis management.

Hematologic malignancies are highly heterogeneous diseases in which the emergence of therapy resistance remains a major obstacle to durable clinical benefit. Cannabinoids, acting through the endocannabinoid system, have drawn increasing interest because of their potential to modulate multiple resistance-associated pathways, yet the available evidence remains fragmented across disease entities, experimental models, and mechanistic frameworks. In this narrative review, we examine the molecular mechanisms by which cannabinoids may counteract drug resistance in leukemia, lymphoma, and multiple myeloma. We discuss their effects on ABC transporter-mediated drug efflux, mitochondrial apoptosis, redox homeostasis, endoplasmic reticulum stress and autophagy, pro-survival signaling, and tumor microenvironment-mediated protection. We also evaluate preclinical evidence for cannabinoid-based combinations with conventional chemotherapy, targeted therapies, immunotherapies, and radiotherapy. Although in vitro and animal studies indicate that cannabinoids may reverse resistant phenotypes and enhance the activity of existing treatments, the translational relevance of these findings is limited by the predominance of cell-line and xenograft models, the paucity of clinical evidence for antitumor efficacy, pharmacokinetic constraints, potential drug–drug interactions, and context-dependent effects that may be neutral or adverse in certain immunological settings. Thus, while the endocannabinoid system represents a potential therapeutic target for sensitizing resistant hematologic malignancies, clinical translation will require validation at pharmacologically achievable exposures, the use of immunocompetent and clinically relevant models, identification of predictive biomarkers, and rigorous evaluation in prospective clinical studies.

Radiation-induced chronic wounds remain a major clinical challenge owing to persistent non-healing and progressive tissue degeneration. Rather than simply representing delayed wound repair, they arise from a self-perpetuating pathological cascade involving DNA damage, oxidative stress, chronic inflammation, microvascular dysfunction, cellular senescence, stem cell impairment, and fibrosis. Current clinical management remains largely supportive and symptomatic, with limited efficacy and no standardized therapeutic regimens targeting the core pathological mechanisms. Emerging strategies—antioxidant, antifibrotic, senolytic, stem cell/exosome-based, and functional biomaterial approaches—show promise. This review critically summarizes recent advances in pathogenic mechanisms and mechanism-based therapeutic strategies, highlighting current translational challenges and future directions for microenvironment-oriented regenerative therapies.