Search Results (2,983)

Essential oils are multicomponent natural products with potential neurobehavioral activity, but integrated comparative studies remain limited. This study compared the essential oils of Satureja brevicalyx, Peperomia dolabriformis, and Rosmarinus officinalis in relation to their chemical profiles, predicted target interactions, preliminary acute oral safety, anxiolytic-like and antidepressant-like effects, antagonist-sensitive behavioral patterns, and exploratory serum biomarkers. Oils were characterized by GC-MS, and their constituents were screened by molecular docking against anxiety-, depression-, sleep-, and stress-related targets. Independent cohorts of male BALB/c mice received oral essential oils (25–100 mg/kg) and were assessed in anxiety-related, depression-related, and locomotor behavioral paradigms, including the elevated plus maze, light–dark box, marble burying, tail suspension, forced swim, and open field tests. Flumazenil and WAY-100635 were used to examine whether the behavioral responses were sensitive to γ-aminobutyric acid type A (GABA-A)/benzodiazepine- and serotonin 1A (5-HT1A)-related pharmacological modulation, respectively. In a preliminary 24-h acute oral toxicity screen, no mortality was observed up to 5000 mg/kg. The three oils produced anxiolytic-like and antidepressant-like effects without reducing spontaneous locomotor activity. Within its experimental block, S. brevicalyx showed the most consistent flumazenil-sensitive anxiolytic-like pattern and FDR-significant reductions in corticosterone and TNF-α, together with increased IL-4. P. dolabriformis showed a broader predicted multitarget docking profile and antagonist-sensitive behavioral attenuation compatible with mixed pathway participation. R. officinalis produced significant but more moderate behavioral effects. WAY-100635 partially attenuated the antidepressant-like effects of all three oils. These findings support differentiated but convergent functional neurobehavioral profiles among the oils. The docking, antagonist, and biomarker results should be interpreted as hypothesis-generating evidence of possible pathway involvement, supporting further validation in chronic stress models, receptor-specific assays, pharmacokinetic studies, and expanded safety evaluations. Full article

Background: The aim of this study was to comprehensively analyze the relationships within a multimodal biomarker panel, including endothelial function indicators, markers of systemic inflammation and myocardial stress, metabolic homeostasis parameters, and an indicator of microstructural damage to nerve tissue in CAD patients with or without type D personality. Methods: This exploratory, cross-sectional, observational study included 72 patients with coronary artery disease. All patients underwent psychological testing (evaluation of type D personality and determination of depression and anxiety levels) and biomarker measurements. The multimodal biomarker panel included measurements of metabolic homeostasis parameters (glucose, total cholesterol, creatinine, insulin, 1,5-anhydroglucitol), markers of systemic inflammation (CRP, IL-6), myocardial stress (NTproBNP), endothelial function parameters (eNOS, EDN1, ADMA, VEGF), and an indicator of microstructural damage to nerve tissue (S100B protein). Results: Biomarker levels revealed no statistically significant differences between the groups with and without personality type D. In personality type D, a direct correlation was found between the level of the brain tissue damage marker S100B and eNOS concentration (R = 0.578; p = 0.006), which was not observed in non-type D. In patients with personality type D, a significant inverse correlation was confirmed between ADMA and creatinine levels (R = −0.524; p = 0.015). In individuals with non-type D personality, a direct correlation was established between total cholesterol levels and VEGF (R = 0.342; p = 0.014). Conclusions: In patients with coronary heart disease, psychological distress (type D) is associated not with an isolated change in biomarker concentrations but with a transformation of the entire structure of their relationships. Personality type D is characterized by a transition from the physiological autonomy of systems to the formation of pathogenetic relationships between them, indicating a decrease in adaptive reserve. Full article

Purpose: This study aimed to develop and validate a comprehensive multi-sensor integrated platform for objective assessment of skeletal muscle recovery kinetics following exercise-induced muscle damage (EIMD), combining biomechanical, thermal, and biochemical monitoring modalities. Methods: Forty elite male athletes were randomized to microwave diathermy (MWD, n = 20, 2.45 GHz, 160 W, 45 min/session) or control (n = 20) groups. Time-synchronized multi-sensor assessments at baseline, 24 h, 48 h, and 72 h post-EIMD included: biomechanical sensors (knee flexion range of motion via goniometry and isokinetic peak torque), thermal sensor (skin surface temperature via infrared thermometry), and biochemical sensor array (serum CK, IL-6, and CRP via high-sensitivity ELISA). Two-way repeated-measures ANOVA with Bonferroni correction examined group × time interactions across all sensor channels. Results: Pre-study validation confirmed high reliability across all sensor modalities. Cross-modality concordance analysis revealed significant correlations between biomechanical and biochemical recovery trajectories (isokinetic torque vs. IL-6: r = −0.73, p < 0.001; pain vs. IL-6: r = 0.68, p < 0.001). MWD intervention demonstrated accelerated recovery across all sensor channels: complete ROM recovery by 48 h (MWDG post-2 vs. baseline, p > 0.05; CG post-3 43% below baseline, p < 0.001), complete isokinetic torque restoration by 72 h (MWDG post-3 vs. baseline, p > 0.05; CG 44% below baseline, p < 0.001), and near-complete pain resolution (VAS 1.70 ± 2.50 mm, p < 0.05). Biomarker sensors demonstrated differential recovery kinetics: IL-6 normalized by 48 h (1.52 ± 0.14 pg/mL, p > 0.05 vs. baseline), CRP approached baseline by 72 h (0.73 ± 0.24 mg/L, p > 0.05), while CK remained elevated at post-3 (169.70 ± 22.58 U/L, 30% above baseline, p < 0.001), indicating incomplete myofiber membrane integrity recovery despite resolution of systemic inflammatory markers. The control group exhibited persistent deficits across all sensor channels with no clinically meaningful recovery. Conclusions: This study validated an integrated multi-sensor platform for recovery assessment. Microwave diathermy demonstrated efficacy by 72 h with complete functional recovery and inflammatory normalization (though CK remained elevated). Cross-modality concordance (r = −0.73 to 0.68) confirmed superior assessment compared to single-modality approaches. This laboratory-based methodology provides a framework for future portable sensor systems in athletic surveillance. Full article

Background/Objectives: Atherosclerotic plaque instability is driven by complex interactions among inflammatory, structural, and cellular remodeling programs. While bulk RNA sequencing provides insight into tissue-level transcriptional states and single-cell RNA sequencing (scRNA-seq) defines cellular heterogeneity, integration across these transcriptomic layers remains limited. We aimed to identify coordinated transcriptional programs associated with stable and unstable plaque phenotypes and map these programs to specific cellular compartments and regulatory networks. Methods: Paired bulk RNA-seq data from stable and unstable human carotid plaques (GSE120521) and scRNA-seq data from human coronary atherosclerotic lesions (GSE131778) were analyzed. Differential expression and Hallmark gene set enrichment analyses were performed using limma and clusterProfiler. Bulk-derived inflammatory and structural signatures were projected onto single-cell data using Seurat module scoring. Compartment-level transcriptional scores, an inflammatory–structural endotype index, and transcription factor activity inference using decoupleR and DoRothEA were used to characterize plaque-associated transcriptional states. Results: Unstable plaques demonstrated enrichment of inflammatory pathways, including interferon gamma response, inflammatory response, TNFα/NF-κB signaling, IL6/JAK/STAT3 signaling, complement activation, and reactive oxygen species pathways. In contrast, stable plaques demonstrated relative enrichment of myogenesis and structural remodeling programs. Projection of bulk-derived signatures onto single-cell data localized inflammatory programs predominantly to TREM2hi and inflammatory macrophage populations, whereas structural programs localized to smooth muscle cell and fibromyocyte-like compartments. Compartment-level analyses showed increased myeloid and adaptive immune signatures in unstable plaques and increased smooth muscle cell/fibro-remodeling signatures in stable plaques. Transcription factor activity analysis identified increased SPI1, NFKB1, RELA, and STAT1 activity in unstable plaques and higher SRF and TEAD1 activity in stable plaques. Conclusions: Integrative analysis of bulk and single-cell transcriptomic data identified distinct inflammatory and structural plaque transcriptional states associated with unstable and stable plaque phenotypes, respectively. These findings support a systems-level framework linking tissue-level plaque behavior to specific cellular and regulatory programs and provide evidence for inflammatory and structural plaque endotypes in human atherosclerosis. Full article

Background/Objectives: Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, is implicated in the pathogenesis of ulcerative colitis (UC). Tryptophan metabolism and its interaction with the aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2–related factor 2 (Nrf2) axis represent a crucial regulatory network in intestinal homeostasis. This study aimed to investigate whether the probiotic fermentation product postbiotic Nagqu4580 alleviates UC by modulating this network to inhibit intestinal epithelial ferroptosis. Methods: An acute UC model was induced in mice using 4% dextran sodium sulfate (DSS). The therapeutic effects of postbiotic Nagqu4580 were evaluated through disease activity index (DAI), colon length, histopathology, inflammatory cytokines, and intestinal barrier function. Ferroptosis was assessed by measuring lipid peroxidation (MDA, 4-HNE), antioxidant capacity (GSH/GSSG), and expression levels of GPX4 and ACSL4. Serum tryptophan metabolites were profiled using targeted metabolomics, the activation of the AhR/Nrf2 pathway was examined by Western blot, immunofluorescence, and qPCR, and gut microbiota composition was analyzed by 16S rRNA sequencing. Results: Postbiotic Nagqu4580 dose-dependently ameliorated DSS-induced UC in mice, as evidenced by reduced DAI scores, mitigated colon shortening and histological damage, decreased inflammatory cytokines (TNF-α, IL-1β, IL-6), and restored intestinal barrier function by upregulating tight junction proteins (Claudin-1, ZO-1, Occludin). Mechanistically, postbiotic Nagqu4580 inhibited intestinal epithelial ferroptosis by reducing MDA and 4-HNE levels, restoring the GSH/GSSG balance, downregulating ACSL4, and upregulating GPX4. Serum metabolomics revealed that postbiotic Nagqu4580 reshaped tryptophan metabolism, increasing beneficial metabolites such as 5-hydroxyindoleacetic acid (5-HIAA) and decreasing potentially harmful metabolites such as 3-indoxyl sulfate (3-IS). 16S rRNA sequencing further revealed that the postbiotic Nagqu4580 partially reversed DSS-induced gut microbiota dysbiosis, with a slight increase in the abundance of beneficial genera and a significant reduction in the abundance of pro-inflammatory genera. Furthermore, postbiotic Nagqu4580 significantly activated the AhR/Nrf2 signaling pathway, enhancing the expression of AhR, Nrf2, and their downstream antioxidant genes HO-1 and GPX4. Conclusions: Postbiotic Nagqu4580 alleviates UC by inhibiting intestinal epithelial ferroptosis. Our data suggest that this protective effect is associated with the remodeling of gut microbiota-related tryptophan metabolism and subsequent activation of the AhR/Nrf2 antioxidant axis. Our findings highlight the therapeutic potential of postbiotic Nagqu4580 as a postbiotic agent for UC. Full article

Lead (Pb) exposure induces liver injury through oxidative stress, inflammation, and gut–liver axis disruption. This study evaluated the protective effects and associated mechanisms of fucoidan (FU) against Pb-induced liver injury in mice. C57BL/6 mice were exposed to lead acetate and treated with FU. High-dose FU (FU-H) improved food intake, body weight, and liver index; decreased Pb levels in serum and liver; and increased fecal Pb content. Compared with the Model group, FU-H reduced serum ALT, AST, and ALP by 54.8%, 38.6%, and 21.7%, respectively. FU-H restored hepatic SOD and GSH by 10.9% and 46.5% and decreased hepatic MDA by 45.9%; it also restored serum SOD and GSH by 30.4% and 24.0%, decreased serum MDA by 19.6%, and suppressed TNF-α, IL-6, and IL-1β by 15.7%, 21.1%, and 14.9%, respectively. Integrated RNA sequencing and network toxicology suggested that insulin-like growth factor-binding protein 1 (IGFBP1) may be associated with FU-mediated protection, and recombinant IGFBP1 partly weakened FU-associated hepatoprotection. Moreover, 16S rRNA sequencing and untargeted metabolomics showed that FU reshaped Pb-disrupted gut microbiota and altered fecal tryptophan metabolism. Exogenous tryptophol supplementation partially alleviated Pb-induced liver injury. Overall, FU protection was associated with reduced Pb burden, IGFBP1-related redox modulation, and gut microbiota-derived tryptophol metabolism. Full article

Background/Objectives: Psoriasis vulgaris is a chronic inflammatory skin condition with significant psychosocial burden. While phototherapy remains one of the most widely used treatment regimens, novel modalities like blue light therapy offer UV-free alternatives with potentially more favorable safety profiles, but their systemic immunomodulatory effects remain poorly understood. We aimed to evaluate the impact of full-body blue light irradiation on clinical outcomes and selected systemic biochemical and immunological markers in patients with mild-to-moderate psoriasis vulgaris. Methods: This preliminary study involved 21 patients (13 females, 8 males) with mild-to-moderate psoriasis vulgaris. Participants received ten sessions of full-body blue light therapy (453 nm, 40 mW/cm², 30 min per session). Clinical assessments (PASI, PGA, DLQI, VAS, Pruritus Scale) and serum analyses of inflammatory (TNF-α, IL-13, IL-17, IL-31), metabolic (adiponectin, 25(OH)D3), and neuroimmune markers (serotonin, kynurenic acid, quinolinic acid) were performed pre- and post-treatment. Results: Significant improvements were observed in PASI, PGA, DLQI, and pruritus scores (p < 0.05). 25(OH)D3, serotonin, and kynurenic acid levels increased significantly, while IL-31 and IL-17 levels decreased and IL-13 levels increased; TNF-α, adiponectin, and quinolinic acid levels showed no significant changes. Counterintuitively, correlation analysis demonstrated a moderate positive association between changes in IL-13 and PASI improvement (r = 0.51, p = 0.02), while changes in other biochemical parameters were not significantly associated with clinical outcomes. Conclusions: Full-body blue light therapy resulted in significant clinical improvement accompanied by heterogeneous systemic immunometabolic changes. These findings suggest complex, pathway-specific immunomodulation, but this requires further investigation in larger controlled studies. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a major global health challenge due to its high prevalence and association with chronic complications, highlighting the need for reliable predictive tools to support clinical decision-making. Methods: This study proposes a two-stage hierarchical prediction system based on a Random Forest (RF) classifier. In Stage 1, the model performs multiclass classification into healthy (H), T2DM without complications (D), and T2DM with complications (C). In Stage 2, patients classified as C are further stratified into microvascular or macrovascular complications. The dataset included 31 biochemical, molecular, inflammatory, and oxidative stress variables from Mexican and Spanish cohorts. Feature selection was performed using Pearson correlation, and feature relevance was further assessed using RF importance measures. Model training used stratified cross-validation, with additional evaluation on a hold-out set to approximate real-world performance. Results: The optimized RF achieved an accuracy of 92% and a macro F1-score of 0.92, outperforming baseline models, with an AUC-ROC of 0.89 for complication prediction. Key predictive features included IL-18, miR-126, duration of T2DM, HbA1c, and IL-10. Conclusions: The novelty of this study lies in integrating heterogeneous biomarkers within a hierarchical predictive framework, rather than in the machine learning algorithm itself. This multimodal approach, combined with interpretable machine learning techniques, is designed to deliver clinically meaningful insights for patient stratification and personalized management in T2DM. Full article

Background/Objectives: Major depressive disorder (MDD) is increasingly recognized as involving inflammation and the microbiota–gut–brain axis. Few studies have simultaneously assessed systemic inflammatory markers and gut microbiota composition within the same cohort while accounting for metabolic confounders. Moreover, data from Middle Eastern and North African (MENA) populations remain limited, restricting our understanding of how diet may influence neuroimmune–microbiome interactions in depression. This study aimed to investigate associations between MDD, systemic inflammatory markers, and gut microbiota composition in Lebanese adults. To our knowledge, this is the first study of its kind in Lebanon, as well as in the MENA region. Methods: In this cross-sectional case–control study, we examined circulating inflammatory markers and gut microbial profiles in 46 adults with DSM-5-confirmed MDD and 25 healthy controls. Plasma C-reactive protein (CRP) and interleukin-6 (IL-6) were measured, and the gut microbiota composition was characterized using 16S rRNA gene sequencing. Multivariable models were adjusted for age, sex, body mass index (BMI), Mediterranean diet adherence, and fluoxetine exposure. Results: Depression status was not independently associated with CRP or IL-6 after adjustment, whereas BMI emerged as a significant determinant of systemic inflammation. At the genus level, MDD was associated with the enrichment of Dorea, Lachnoclostridium, Collinsella, Bilophila, and Klebsiella and the depletion of Christensenella, Mitsuokella, and Victivallis, independent of inflammatory biomarkers. Alpha diversity did not differ between groups, while beta diversity showed modest metric-dependent differences, primarily driven by presence/absence-based measures. Conclusions: Specific microbial taxa may contribute to gut–brain signaling pathways implicated in MDD and systemic inflammation. Further longitudinal and mechanistic studies are required to clarify causal interactions within inflammation–microbiome networks in MDD. Full article

Background/Objectives: Severe asthma and chronic rhinosinusitis with nasal polyps (CRSwNP) frequently coexist and are associated with type 2 inflammation, leading to poor symptom control and high healthcare burden. Biologic therapies targeting IL-4Rα and IL-5/IL-5R have shown efficacy in type 2 inflammatory asthma and CRSwNP, but comprehensive evidence on their efficacy, safety, and research trends is limited. Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating dupilumab, mepolizumab, benralizumab, or reslizumab in patients with type 2 inflammatory asthma and/or CRSwNP. Primary outcomes included lung function (FEV1), symptom control (ACQ, SNOT-22, nasal polyp score), and serious adverse events (SAEs). Risk of bias was assessed using the Cochrane RoB 2.0 tool. Publication bias was evaluated with funnel plots and Trim-and-Fill analysis. Bibliometric analysis was performed to identify publication trends and emerging research directions. Results: A total of 23 RCTs involving 8758 participants were included. Biologic therapy was not associated with a significant increase in serious adverse events (RR = 1.15, 95% CI: 0.89–1.50). Compared with control treatment, biologics significantly improved FEV1 (MD = 100.67 mL, 95% CI: 65.94–135.40) and ACQ scores (MD = −0.40, 95% CI: −0.54 to −0.25). In patients with CRSwNP and comorbid asthma, biologics also improved SNOT-22 scores (MD = −13.16, 95% CI: −24.85 to −1.47) and nasal polyp scores (MD = −1.31, 95% CI: −1.95 to −0.68). Dupilumab trials showed larger reductions in nasal polyp score than IL-5/IL-5R-targeted trials, although this indirect comparison should be interpreted cautiously. Bibliometric analysis indicated increasing research attention to upstream epithelial targets such as TSLP. Conclusions: Both IL-4Rα and IL-5/IL-5R-targeted biologics are effective and well-tolerated in type 2 inflammatory airway diseases. IL-4Rα inhibition shows favorable upper-airway outcomes in CRSwNP with asthma, but head-to-head trials are needed to clarify its comparative efficacy relative to IL-5/IL-5R-targeted therapies. Emerging research directions are shifting toward upstream epithelial alarmin antibodies. Full article

In patients with myocardial infarction (MI), the level of sphingolipids, such as ceramide (Cer), is elevated and is associated with an increased risk of progression towards heart failure (HF). Dihydroceramide desaturase 1 (DES1) catalyses the conversion of dihydroceramide (dhCer) into Cer in the de novo sphingolipid pathway. While pharmacological inhibition of DES1 has shown therapeutic benefits in metabolic disease and cancer models, its role in cardiac remodelling remains unclear. This study aimed to determine whether pharmacological inhibition of DES1 using the novel compound, CIN038, attenuates cardiac remodelling following ischemia–reperfusion (I/R) injury. Three-month-old male C57Bl/6 mice underwent I/R or sham surgery (n = 8) and were treated with vehicle or CIN038 (50 mg/kg/day, i.p.) for 28 days. Cardiac function, molecular changes, and lipid profiles in circulation and liver were assessed at the endpoint. CIN038 reduced infarct size and cardiac myocyte hypertrophy compared to the I/R + vehicle group. Profibrotic signalling was reduced in the infarcted hearts, as evidenced by reduced expression of Col1a1, Col3a1, and Tgfb mRNA and decreased levels of α-SMA and TGFβ1 protein expression. Inflammatory signalling was attenuated with reduced ERK and NFkB phosphorylation and suppression of Il-6-STAT axis. Despite these structural and molecular improvements, no changes were observed in cardiac function. Lipidomic analysis revealed selective alterations in circulating and hepatic lipid species, including plasmalogen phosphatidylethanolamines and ether-linked triglycerides, suggesting modulation of lipid metabolism. Collectively, these findings indicate that CIN038 attenuates post-ischemic cardiac remodelling by suppressing inflammatory and profibrotic signalling, highlighting DES1 as a potential therapeutic target following MI. Full article

Imiquimod-induced skin inflammation is the most widely used psoriasis mouse model. Although p38 mitogen-activated protein kinase reportedly plays a role in the pathogenesis of psoriatic inflammation, the purpose of one of its upstream activators, apoptosis signal-regulating kinase 1 (ASK1), remains unclear. This study investigated the role of ASK1 and its molecular mechanism in the imiquimod-induced psoriasis model. Compared to wild-type mice, the ASK1 knockout (KO) mouse skin lesion showed a higher clinical score and a thicker epidermis. The mRNA expression of pro-inflammatory cytokines, such as IL-17 and TNF-α, was also higher. Notably, the expression of aryl hydrocarbon receptor (AhR), a sensor for xenobiotic chemicals that is expressed in the skin to strengthen the skin barrier and accelerate terminal differentiation of the epidermis—as well as its downstream molecule CYP1A1, but not NRF2—was increased in the ASK1 KO psoriatic skin lesion. Immunoprecipitation analysis, followed by Western blotting, revealed that ASK1 interacts with AhR in cells transfected with their respective expression vectors, potentially leading to reduced AhR expression. These results suggest that ASK1 negatively regulates the development of the imiquimod-induced mouse psoriasis model by interacting with AhR and presumably antagonizing the AhR-CYP1A1 axis. Full article

This study investigated the protective effects of DBD against Staphylococcus aureus (S. aureus)-induced mastitis in mice and explored whether these effects were associated with gut microbiota alterations, blood–milk barrier integrity, and inflammatory signaling. A lactating mouse model of mastitis was established, and the effects of DBD were evaluated using HPLC, histopathological analysis, ELISA, qRT-PCR, Western blotting, immunofluorescence, and 16S rRNA sequencing. The results showed that DBD significantly reduced bacterial loads in mammary tissues, decreased the expression of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, and alleviated inflammatory cell infiltration and tissue damage. Moreover, DBD upregulated the expression of tight junction proteins and improved the integrity of the blood–milk barrier. DBD treatment was also associated with alterations in gut microbiota composition, as reflected by changes in the relative abundance of several bacterial taxa. In addition, DBD inhibited the activation of the NF-κB/NLRP3 and MAPK inflammatory signaling pathways. Collectively, these findings indicate that DBD alleviates S. aureus-induced mastitis accompanied by alterations in gut microbiota composition, suppressing inflammatory responses, and repairing the blood–milk barrier, suggesting its potential as a therapeutic agent for mastitis. Full article

Background: Cytarabine (Ara-C) remains the cornerstone of remission-induction and consolidation chemotherapy for acute myeloid leukemia (AML) and related hematological malignancies. Despite more than six decades of clinical use, its multi-organ toxicity continues to be managed almost exclusively through dose attenuation and supportive care, with no approved upstream pharmacological prevention strategy available. Objectives: This scoping review aimed to systematically map the breadth and nature of pharmacological agents tested in vivo for their capacity to mitigate cytarabine-induced multi-organ toxicity, to characterize their mechanisms of action and organ targets, and to identify evidence gaps and agents with translational potential. Methods: The review was designed and reported in accordance with the PRISMA-ScR checklist. A structured electronic search was conducted across PubMed/MEDLINE, Scopus, Cochrane Library and Embase, and Web of Science from database inception to 15 July 2025. Eligible studies were restricted to full-text, peer-reviewed, English-language research involving in vivo mammalian models administered cytarabine as the principal toxin, with at least one pharmacological co-intervention and at least one quantitative or histopathological organ-injury outcome. Results: From 5701 retrieved records, 36 eligible in vivo mammalian studies (spanning 1964–2024) were identified. Included studies addressed neurotoxicity (n = 6), gastrointestinal mucositis (n = 9), ocular toxicity (n = 3), hepatotoxicity (n = 3), bone marrow suppression (n = 4), chemotherapy-induced alopecia (n = 5), and reproductive and developmental toxicity (n = 4). Five recurring mechanistic strategies were identified across the heterogeneous agents tested: redox buffering (N-acetylcysteine, α-lipoic acid, rutin, swertiamarin, α-tocopherol), mitochondrial preservation (betanin, thymoquinone, vitamin D, sodium zinc dihydrolipoylhistidinate [DHLHZn]), tissue-microenvironment reprogramming (apraglutide, BADGE, plerixafor, short-chain fatty acids, β-glucan), molecular antagonism (deoxycytidine, dCMP), and immunomodulation (lienal peptide, IL-1β, AHCC). Conclusions: This scoping review provides the first systematic cartography of pharmacological mitigation strategies for cytarabine-induced multi-organ toxicity. Five mechanistic pathways converge across eight organ systems, with apraglutide and N-acetylcysteine representing the most clinically translatable candidates. Plerixafor and PPARγ blockade by BADGE constitute high-priority candidates for bone marrow niche protection, while the deoxycytidine antagonism principle warrants formal pharmacokinetic evaluation. The complete absence of cardiotoxicity mitigation data defines the most critical gap for future research. Full article

Background: A complex interplay between viral activity and host immune responses drives the progression of liver fibrosis in chronic hepatitis B. The T helper 17 (Th17) immune pathway, which produces the pro-inflammatory cytokine interleukin-17A (IL-17A), has been implicated in hepatic fibrogenesis. However, the relationship between IL-17A levels, IL-17A G197A (rs2275913) gene SNP, and the degree of liver fibrosis across different phases of the natural history of chronic hepatitis B remains insufficiently explored. Methods: This study employed an analytical observational design with a cross-sectional approach in treatment-naïve patients with chronic hepatitis B. The degree of liver fibrosis was assessed using liver elastography. IL-17A (rs2275913) gene SNP was analysed using Real-Time PCR, while serum IL-17A levels were measured using enzyme-linked immunosorbent assay. Statistical analyses included Spearman’s correlation, the contingency coefficient, the Chi-square test, the Kruskal–Wallis test, and the Mann–Whitney test, with a significance level set at p < 0.05. Results: A total of 76 patients with chronic hepatitis B were included in this study. The phase of disease progression was significantly associated with the degree of liver fibrosis (p = 0.016). Median IL-17A levels increased in parallel with fibrosis severity (p = 0.003), with a particularly significant association observed during the R phase (p = 0.002). However, no significant association was found between the IL-17A G197A (rs2275913) gene SNP and either liver fibrosis severity or serum IL-17A levels. Conclusions: Elevated serum IL-17A levels were associated with greater liver fibrosis severity, particularly during the reactivation phase of chronic hepatitis B. These findings suggest a potential relationship between IL-17A-mediated immune responses and liver fibrosis in patients with chronic hepatitis B. Full article