Background: Social isolation (SI) is a long-standing experimental paradigm that models schizophrenia-like behavioural and neurobiological changes caused by the action of oxidative stress, neuroinflammation, apoptosis, and neurotransmitter imbalance. The scope of this paper was to comparatively assess the effectiveness of rutin, sodium selenite (Na ₂ SeO ₃ ), and rutin-conjugated selenium nanoparticles (RUT-SeNPs) to determine their neuroprotective activity using a rat model of neurobehavioral impairment following SI. Methods: In silico analysis of Rutin activity including in silico ADMET and toxicity, and molecular docking. Forty-two healthy male albino rats were allocated equally in to six groups; Control group, Social isolation group (SI), SI treated with Olanzapine (SI&OLA), SI treated with Rutin group (SI&RUT), SI treated with the sodium selenite group (SI&Na ₂ SeO ₃ ), and SI treated with Se nanoparticles biosynthesized using the Rutin group (SI&RUT-SeNPs). All groups undergone biochemical analysis including behavioral tests, assessment of neural function, oxidative stress, inflammation, and apoptosis, histopathological analysis, immunohistochemistry, and gene expression. Results: SI induction produced significant behavioral, biochemical, neurochemical, and structural impairments compared with controls ( P < 0.05). SI rats showed marked reductions in locomotion, sucrose preference, social interaction, antioxidant capacity (Nrf2, SOD, CAT, GSH), neurotransmitters (serotonin, dopamine, GABA, glycine), and BDNF, alongside significant increases in oxidative stress markers (8-OHdG, MDA, NO), inflammatory cytokines (TNF-α, IL-1β, NF-κB), apoptotic mediators (Bax and Caspase-3), GFAP, and histological degeneration ( P < 0.05). Across all assessments, RUT-SeNPs produced the strongest and statistically significant recovery, yielding values comparable to control and significantly superior to SI, SI&OLA, and SI&RUT groups ( P < 0.05). RUT-SeNPs normalized behavioral outcomes, antioxidant status, cytokine levels, apoptotic markers, neurotransmitters, BDNF/GFAP balance, and cortical histoarchitecture. Conclusion: Rutin and sodium selenite provided significantly protective effects across behavioral, biochemical, and neurochemical parameters. Among all treatments, RUT-SeNPs produced markedly attenuated, restoring nearly all measured markers including redox balance, cytokines, apoptosis regulators, neurotransmitters, BDNF/GFAP levels, and cortical histology to values comparable to controls.

Bone fractures remain a significant clinical challenge, with current treatments often facing limitations. This study investigated the potential of ulvan-mediated biogenic selenium nanoparticles (Ulvan-SeNPs) to enhance bone fracture healing through osteoinductive, anti-inflammatory, and antioxidant mechanisms. A standardized mid-diaphyseal femoral fracture was induced in a rat model. Rats were orally administered Ulvan, Na ₂ SeO ₃ , or Ulvan-SeNPs. Fracture healing was assessed using radiographic, biochemical (inflammatory markers: NF-κB, IL-1β, TNF-α, CRP; antioxidant enzymes; bone turnover markers: ALP, osteocalcin, CTX-II), and histological analyses (PCNA, TGF-β expression, tissue organization). Radiographic data indicated superior healing in the Ulvan-SeNPs group, characterized by near-complete fracture line obliteration, substantial callus development, and significant remodeling. Biochemically, the Ulvan-SeNPs group exhibited a significant decrease in inflammatory indicators and an increase in antioxidant enzyme activities and bone turnover markers. Histological and immunohistochemical analyses further supported these findings, revealing significant PCNA and TGF-β expression, minimal fibrous tissue, well-organized new trabecular bone, and robust endochondral ossification in the Ulvan-SeNPs group. These findings demonstrate that the Ulvan-SeNPs conjugate significantly promote bone regeneration by stimulating cellular proliferation and osteogenesis, enhancing antioxidant defence, and modulating inflammatory responses. This suggests Ulvan-SeNPs as a promising therapeutic agent for bone fracture repair.

Objective: This review aims to highlight the biological characteristics of mesenchymal stem cells (MSCs) and their derived exosomes, focusing on their therapeutic roles in liver diseases and cancer. Material and Methods: A comprehensive literature review was conducted to evaluate MSC sources, isolation methods, and the biological functions of MSC-derived exosomes. Relevant experimental and clinical studies addressing their mechanisms of action in liver pathology and cancer were analysed. Results: MSCs and their exosomes demonstrated significant potential in modulating immune responses, reducing inflammation and fibrosis, promoting hepatocyte regeneration, and influencing the tumour microenvironment. MSC-derived exosomes also showed advantages as cell-free therapeutic agents and targeted drug delivery systems due to their low immunogenicity and biological stability. Conclusion: MSCs and MSC-derived exosomes represent promising therapeutic platforms for regenerative medicine and cancer treatment, with strong potential for future clinical translation.

Chemotherapy remains foundational to oncology, yet treatment response, resistance, and gastrointestinal toxicity vary widely between patients in ways that tumor stage, molecular subtype, and host pharmacogenomics do not fully explain. The gut microbiome contributes to this variability through two primary mechanisms: direct biotransformation and bioaccumulation of cytotoxic agents by microbial enzymes, and indirect modification of epithelial barrier integrity, inflammatory tone, and ecological resilience after cytotoxic injury. We propose precision pharmacomicrobiomic conditioning: the drug-specific, timing-anchored preservation or reshaping of microbial function before and during chemotherapy, which is distinguished from generic microbiome modulation by its linkage to a defined pharmacologic and toxicity profile. We operationalize this concept through two original constructs: five-archetype baseline risk classification stratifying patients by microbial enzymatic, inflammatory, ecological, and recovery phenotypes; and a three-phase clinical workflow specifying the assay, time point, and decision rule from pre-treatment stratification through adaptive longitudinal monitoring. These constructs are proposed strictly for prospective validation and are not presented as clinically validated decision tools. Furthermore, while dynamic functional and metabolic biomarkers may have higher predictive value than static, single bacterial taxa, this hypothesis requires rigorous confirmation in sufficiently powered, externally validated clinical cohorts. We conclude with the minimum reporting standards required to test these constructs: chemotherapy exposure metrics, toxicity grading versions, functional and strain-level profiling, and engraftment endpoints, and position microbiome profiling as an additional stratification layer integrated with pharmacogenomics and conventional clinical predictors, not as independent grounds for dose modification. Currently, no microbiome-derived biomarker has undergone prospective validation or received regulatory approval for standard chemotherapy stratification.

Monoamine oxidase B (MAO-B) is a clinically validated target in Parkinson’s disease (PD), but docking rank alone is insufficient to establish a CNS-directed inhibitor. We integrated MAOB-related pathway context, domain-resolved structural annotation, GNINA virtual screening, predicted blood–brain barrier (BBB) permeation, molecular dynamics (MD), density functional theory (DFT) and ADMET assessment to nominate hypothesis-stage computational candidates. A pharmacophore-derived input collection 2870 entries was subjected to virtual screening; a curated BBB-positive, favorable Vina/CNN-affinity shortlist yielded PubChem CIDs 143667968, 42876521 and 1232631. The three candidates had similar reported GNINA scores. In single 100 ns MD trajectories, CID 42876521 displayed frequent protein–ligand hydrogen bonds, whereas CID 143667968 displayed almost none and reduced aromatic-cage fluctuation. CID 143667968 also had the smallest gas-phase HOMO–LUMO gap. All three compounds carried predicted mutagenicity, carcinogenicity and hERG alerts. CID 42876521 is therefore prioritized for validation, CID 143667968 is retained as a complementary hypothesis and CID 1232631 as a backup scaffold. These results define a preliminary, multi-parameter prioritization framework.