Search Results (854)

Metabolic dysfunction-associated steatohepatitis (MASH; formerly non-alcoholic steatohepatitis, NASH) is characterized by oxidative stress, inflammatory activation, hepatocellular injury, and progressive liver dysfunction. However, the global transcriptomic landscape underlying stress-induced hepatic injury remains incompletely understood. In this study, we employed a methionine–choline-deficient (MCD) diet-induced murine model to characterize the phenotypic and transcriptomic alterations associated with liver injury. Male C57BL/6J mice were fed either a control or MCD diet, and hepatotoxicity was assessed by survival analysis, body and liver weight measurements, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, histopathological examination, RNA sequencing, quantitative real-time PCR (qRT-PCR), and tumor necrosis factor-alpha (TNF-α) enzyme-linked immunosorbent assay (ELISA). MCD feeding markedly reduced survival and body weight while inducing hepatomegaly and significant elevations in serum ALT and AST, indicating severe hepatocellular injury. Histopathological analysis demonstrated hepatic steatosis, hepatocellular ballooning, and lobular inflammation without histological evidence of fibrosis. Transcriptomic profiling revealed extensive gene expression remodeling, characterized by activation of inflammatory pathways, enrichment of MAPK-related signaling, dysregulation of lipid metabolism, suppression of antioxidant defense systems, impairment of cytochrome P450-mediated detoxification, and upregulation of apoptosis-associated genes. qRT-PCR further validated the differential expression of representative genes involved in inflammatory signaling (Tlr4, Nfkb1, Nlrp3, and Casp1), MAPK signaling (Fos), xenobiotic metabolism (Cyp4f18), lipid metabolism (Apoa4 and Lpl), extracellular matrix remodeling (Mmp12), and oxidative stress responses (Sod1 and Gstp1). In addition, elevated serum TNF-α levels provided protein-level evidence supporting activation of the TLR4/NF-κB/TNF-α/NLRP3 inflammatory axis. Although fibrosis-associated transcriptional responses were detected, the absence of histological fibrosis suggests transcriptional priming of fibrogenic pathways rather than established fibrogenesis. Collectively, these findings provide a transcriptomic framework linking oxidative stress, impaired detoxification, inflammatory activation, and stress-responsive signaling to MCD-induced hepatic injury. The MCD model provides a valuable experimental platform for characterizing hepatic stress-response transcriptomes and for generating hypotheses that can subsequently be evaluated in environmentally relevant toxicological models. Nevertheless, caution should be exercised when extrapolating these findings to obesity-associated human MASLD, as the MCD model lacks key metabolic features of the human disease, including obesity and insulin resistance. Therefore, the present findings should be interpreted primarily as transcriptomic signatures of stress-induced hepatic injury rather than as a direct representation of the pathophysiological processes underlying human obesity-associated MASLD. Full article

Glioblastoma multiforme (GBM), isocitrate dehydrogenase (IDH)-wildtype, is the most aggressive primary malignant tumor of the central nervous system, characterized by poor prognosis and high recurrence rates despite standard multimodal treatment. This study investigates the molecular response of glioblastoma cells to 5-aminolevulinic acid (5-ALA)-based photodynamic therapy (PDT), focusing on gene expression changes associated with apoptosis, ferroptosis, and oxidative stress. Human glioblastoma T98G cells were treated with 5-ALA followed by light irradiation, and gene expression was analyzed using RT-qPCR. PDT induced moderate upregulation of pro-apoptotic genes (BAX, CASP3, FAS) alongside increased expression of the anti-apoptotic gene BCL2, indicating simultaneous activation of cell death and survival pathways. Ferroptosis-related genes showed mixed responses, with slight upregulation of ACSL4 and downregulation of GPX4, suggesting increased susceptibility to lipid peroxidation. The most significant change was observed in GCH1 expression, reflecting activation of oxidative stress response mechanisms. However, none of the observed changes reached statistical significance, likely due to the limited sample size. These findings demonstrate that PDT induces a complex and dual biological response in glioblastoma cells, involving both cytotoxic and adaptive mechanisms. This may limit therapeutic efficacy and contribute to treatment resistance. The results support the rationale for combining PDT with targeted molecular therapies aimed at inhibiting antioxidant defenses and anti-apoptotic pathways. Additionally, personalized therapeutic strategies based on tumor molecular profiles may enhance treatment outcomes. Further studies with larger sample sizes and functional validation are required to confirm these preliminary observations. Full article

Global warming has increasingly positioned heat stress (HS) as a major threat to public health, as it can inflict damage on multiple organs including the kidneys, liver, and heart. However, effective targeted therapeutic strategies remain limited. This investigation employed an integrated approach combining Network pharmacology, in silico binding simulations, and cell-based assays to elucidate the cytoprotective properties and molecular basis of oxymatrine action under heat-stressed conditions. Network analysis identified 36 overlapping targets common to oxymatrine and the pathological processes of HS-related acute kidney injury (AKI), acute liver injury (ALI), and acute myocardial injury (AMI). These targets were strongly enriched in the PI3K-AKT signaling cascade. Molecular docking showed that oxymatrine binds tightly to key pathway proteins such as PIK3CA and GSK3B, with Vina scores below −8 kcal/mol. In 293T cells, the half-maximal cytotoxic concentration (CC₅₀) of oxymatrine exceeded 2000 μM. Under heat stress, oxymatrine (31.25–1000 μM) dose-dependently increased cell viability by about 30% and significantly lowered HSP90 and HSP70 expression. Similar protective effects were observed in H9C2 cardiomyocytes under heat stress. RT-qPCR further confirmed that oxymatrine reduced the transcript levels of PI3K-AKT pathway-related genes, including CASP3, EGFR, RXRα, and MMP9 in 293T cells. We also found 18 overlapping targets between oxymatrine and ferroptosis, most of which matched the core targets above. Molecular docking analysis predicted binding of oxymatrine to the ferroptosis regulator GPX4. Together, these results suggested that oxymatrine potentially alleviates HS injury by modulating the PI3K-AKT signaling pathway andregulating potential ferroptotic targets such as GPX4. Full article

Background/Objectives: Registered nurse (RN) prescribing is increasingly discussed as a strategy to improve primary-care access, medication follow-up, chronic disease management, and service responsiveness. The available evidence, however, does not directly test a single coordinated RN prescriber–family physician/nurse practitioner (FP/NP) model. This integrative review synthesized heterogeneous evidence relevant to how RN prescribing may be organized within team-based primary care. Methods: A structured integrative review approach was used to map evidence from nurse and non-medical prescribing, RN-led primary care, nurse–physician substitution, interprofessional collaboration, chronic disease medication titration, patient-experience, and implementation research. Searches completed on 30 March 2026 included PubMed/MEDLINE, PubMed Central, the Cochrane Library search interface, publisher full-text platforms, targeted scholarly searches, citation chasing, and Canadian regulatory/professional sources. Methodological quality was appraised using AMSTAR 2- and CASP-informed criteria, and the strength of interpretation was assessed narratively. No meta-analysis was performed because of substantial heterogeneity and the risk of double-counting primary studies included in prior evidence syntheses. Results: A total of 286 records were identified. After de-duplication, screening, and eligibility assessment, 37 peer-reviewed records were included: 30 review-level or evidence-synthesis records and 7 primary, mixed-methods, or patient-experience studies. Four official regulatory/professional sources were retained separately for context. Nurse and non-medical prescribing were generally associated with comparable or favourable outcomes for blood pressure, glycated hemoglobin, low-density lipoprotein cholesterol, medication adherence, patient satisfaction, and selected access outcomes in defined contexts. Direct evidence for the exact RN prescriber–FP/NP configuration remains limited. Conclusions: Current evidence is consistent with a coordinated RN prescribing model embedded within primary-care teams, but does not establish causal superiority of this configuration over other models. Coordinated RN prescribing should therefore be understood as an evidence-informed and testable implementation model requiring prospective evaluation, particularly for diagnostic safety, adverse events, continuity, workload, cost, and patient-level outcomes. Full article

The Houpoea officinalis flower (HOF) represents an underutilized sustainable bio-resource. This study systematically evaluated its potential using an ethanol-based green extraction process optimized by Response Surface Methodology, with the optimal conditions consisting of approximately 50% ethanol, a solvent-to-solid ratio of 54 mL/g, and an extraction time of 31 min. Chemical profiling across four developmental stages—S1 (Bud), S2 (Bud swelling), S3 (Initial flowering), and S4 (Full bloom)—suggested magnolol and honokiol as the major phenolic compounds, showing a trend of decline during early development followed by an increase at the S4 stage. A significant positive correlation was observed between total phenolic content and antioxidant activity, and the S1 stage extract displayed the strongest antioxidant capacity in multiple in vitro assays. Network pharmacology analysis predicted oxidative stress-related targets and pathways, with TP53, AKT1, IL6, BCL2, and CASP3 recognized as key hub genes. Molecular docking further predicted favorable binding interactions between major HOF phenolics and these target proteins. Collectively, these findings reveal the multi-target antioxidant potential of HOF and provide evidence supporting its potential role in antioxidant-related traditional applications based on predicted mechanisms. Moreover, HOF, particularly at the S1 developmental stage, shows promise as a sustainable source of natural antioxidants and functional ingredients, promoting the high-value utilization of agricultural by-products. Full article

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are characterized by substantial biological heterogeneity and complex regulation of apoptosis, metabolism, and angiogenesis. The aim of this study was to evaluate the concentrations of selected proteins: FGF2, HGF, Fas/CD95, CASP9, ALDH1A1, and GLUT1 in tumor and margin samples and assess correlations with clinical and demographic parameters. A total of 59 samples from patients with GEP-NETs were analyzed using multiplex immunoassay and ELISA methods. Significant differences in protein expression between tumor and margin tissues were observed. Fas/CD95 levels were lower in tumor samples, whereas HGF concentration was higher. Elevated HGF, FGF2 and Fas/CD95 levels were associated with advanced tumor stage. HGF and GLUT1 concentrations varied depending on nodal status, while FGF2, Fas/CD95, and CASP9 levels were increased in metastatic cases. Additionally, differences related to tumor localization and the influence of smoking and alcohol consumption were identified. Dysregulation of apoptotic, metabolic, and angiogenic pathways plays a crucial role in GEP-NETs progression and highlights the importance of the tumor microenvironment. GEP-NET exhibit biological heterogeneity and complex progression driven by multiple interacting molecular pathways. The factors analyzed may have potential significance as biomarkers of disease progression; however, their exact role requires further investigation in larger, prospective cohorts. Full article

Glioblastoma multiforme (GBM) remains one of the most aggressive primary brain tumors with poor prognosis despite multimodal therapy. Photodynamic therapy (PDT) using indocyanine green (ICG) is an emerging adjuvant approach aimed at eliminating residual tumor cells after resection. While ICG-PDT exerts cytotoxic effects, its impact on molecular pathways regulating programmed cell death in glioma cells is not fully understood. In this study, T98G and U-118MG glioblastoma cells were divided into four groups: untreated control, light-only (10 min broadband irradiation), ICG-only (15 min incubation), and ICG-PDT (15 min ICG + 10 min broadband irradiation). Relative mRNA expression of apoptosis-related genes (BAX, BCL2, CASP3, FAS) and ferroptosis-related genes (GPX4, ACSL4, SLC7A11, GCH1) was quantified 24 h post-treatment by RT-qPCR using the 2^−ΔΔCt method. ICG-PDT significantly reduced cell viability to 67.79% ± 3.39% (vs. 86.66% ± 4.33% in control), confirming effective phototoxicity. No statistically significant differences in mRNA levels were observed for any of the investigated genes across the groups (one-way ANOVA and Kruskal–Wallis, all p > 0.05). The largest non-significant deviation was a mild decrease in GPX4 (fold change 0.87) in the ICG-PDT group. Fluctuations in GCH1 were accompanied by high variance, likely reflecting technical noise rather than a true biological trend. The mRNA BAX/BCL2 ratio remained stable (~30) across all conditions. In contrast, the U-118MG line showed greater transcriptional sensitivity, with statistically significant decreases in CASP3 (p = 0.012) and ACSL4 (p = 0.031) expression, along with downward trends in BCL2 and GPX4 following ICG-PDT. ICG-PDT does not induce significant transcriptional changes in the analyzed genes T98G at the 24 h time point under the applied experimental conditions. In U-118MG cells, moderate transcriptional engagement of both apoptotic and ferroptotic routes was observed. Further studies at the protein and functional levels, across multiple time points and models, are warranted to fully elucidate the mechanisms of ICG-PDT in glioblastoma. Full article

Renibacterium salmoninarum, the etiological agent of bacterial kidney disease, is a facultative intracellular pathogen whose interaction with salmonid phagocytic cells remains poorly resolved at the protein level. Here, we aimed to define the temporal protein-abundance architecture of SHK-1 macrophage-like cells after R. salmoninarum inoculation and to test whether this response supports broad canonical cell-death pathway engagement. We used label-free quantitative LC-MS/MS proteomics to profile SHK-1 cells over a 48 h post-inoculation time course. Because the design included a single non-infected T0 baseline, analyses were framed as baseline-referenced post-inoculation comparisons rather than a fully controlled mock time course. Of 6842 proteins retained for statistical modeling, 2254 were strictly differentially abundant in at least one contrast relative to T0 (adjusted p < 0.05 and |log₂FC| ≥ 0.585). Perturbation was strongest at 1–2 h and progressively contracted at later time points. Among 1278 recurrent proteins, k-means clustering resolved four temporal modules capturing coordinated remodeling of lysosomal, immunometabolic, cytoskeletal, stress-response, and antioxidant programs. A curated cell-death panel spanning apoptosis, pyroptosis, necroptosis, ferroptosis, and PANoptosis yielded only three detected markers; CASP3 and MLKL met the strict threshold, whereas ACSL4 remained sub-threshold. Overall, early host-cell remodeling, rather than broad canonical death-program execution, was the predominant proteomic signature of SHK-1 cells during the first 48 h after R. salmoninarum inoculation. Full article

Background: The NLRP3 inflammasome is a key driver of obesity-associated chronic low-grade inflammation, contributing to hypothalamic neuroinflammation and disruption of energy homeostasis. Quercetin, a bioactive flavonoid, has been proposed as a modulator of inflammatory and metabolic pathways, including the fat mass and obesity-associated gene (FTO). Objective: This study evaluated the effects of quercetin on hypothalamic mRNA expression of Fto and components of the TNF-α/NF-κB/NLRP3 pathway. Methodology: In a high-fat diet (HFD)-induced obesity model, male Wistar rats (n = 18) were divided into three groups: standard diet (SD), HFD, and HFD + Q (supplemented with quercetin 50 mg/kg/day for 12 weeks). Gene expression was analyzed by quantitative PCR using the 2^−ΔΔCt method. Results: HFD significantly increased the expression of Fto and pro-inflammatory genes, including Tnf, Nlrp3, Casp1, Il1b, and Il18. Quercetin supplementation attenuated this upregulation, restoring expression levels toward baseline. Conclusions: These findings indicate that quercetin reduces hypothalamic neuroinflammation and modulates Fto expression, likely through inhibition of NF-κB signaling and suppression of NLRP3 inflammasome activation. Quercetin may represent a potential molecular modulator of obesity-associated neuroinflammatory processes. Full article

Pubertal initiation critically determines reproductive performance in female pigs. Histone H3 lysine 27 trimethylation (H3K27me3) has been implicated in ovarian development. However, its genome-wide regulatory landscape during the pubertal transition remains unexplored. Here, we obtained transcriptomes of GCs treated with the pharmacological H3K27me3 agonist GSK-J4 or H3K27me3 inhibitor EPZ005687. We found that H3K27me3 substantially remodels the transcriptomic landscape of porcine GCs, with differentially expressed genes significantly enriched in pathways governing cell proliferation and apoptosis. Mechanistically, H3K27me3 suppressed GC proliferation by downregulating the expression of PCNA and promoting apoptosis through upregulation of CASP3, thereby delaying pubertal initiation. Furthermore, genome-wide ChIP-seq analysis on porcine ovaries from pre-pubertal and in-pubertal gilts revealed higher H3K27me3 enrichment around transcription start sites in the In-puberty stage than in the Pre-puberty stage. Genes with promoters exhibiting reduced H3K27me3 occupancy during the pubertal transition were enriched in pathways related to sex differentiation and serine-type endopeptidase inhibitor activity. Notably, secretory leukocyte peptidase inhibitor (SLPI) was identified by ChIP-qPCR as a direct target repressed by H3K27me3. Functional validation demonstrated that SLPI promoted GC proliferation and inhibited GC apoptosis in vitro. Intraperitoneal injection of LV-Slpi or sh-Slpi into C57BL/6J mice showed that Slpi accelerated pubertal initiation of mice in vivo. Collectively, our findings confirmed that developmental stage-specific loss of H3K27me3 at the SLPI promoter derepressed SLPI transcription, which in turn promoted porcine GC proliferation, suppressed apoptosis, and facilitated pubertal initiation in mice. These results provided valuable insights into the epigenetic regulation of pubertal initiation in mammals. Full article

Aim: Self-stigma represents a major barrier to recovery among individuals with severe mental illness (SMI). This review aimed to identify and synthesize the available evidence on the effectiveness of non-pharmacological interventions for reducing self-stigma in adults with SMI, while also exploring physical appearance care as a potentially relevant but under-researched area. Methods: A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines and the Cochrane Handbook recommendations. The review protocol was registered in PROSPERO (CRD420251013333). Data Sources: A comprehensive search was conducted across multiple databases, including the Virtual Health Library, PubMed, Web of Science, the Cochrane Library, and EBSCOhost databases. A snowball search of reference lists was also performed. Studies published in English or Spanish within the past ten years were included. Review Methods: Two independent reviewers screened titles, abstracts, and full texts according to predefined criteria. Methodological quality was assessed using the Critical Appraisal Skills Programme España (CASPe). A qualitative synthesis was conducted for all included studies, and a random-effects meta-analysis was performed for studies providing sufficient quantitative data. Standardized mean differences and heterogeneity statistics were calculated. Results: Twenty-eight studies were included in the qualitative synthesis, and twelve were eligible for meta-analysis. Multicomponent interventions integrating psychoeducation, cognitive restructuring, narrative approaches, and social support showed the most consistent effects across the evaluated outcome domains. Meta-analytic findings indicated small-to-moderate reductions in self-stigma and improvements in hope, with low levels of statistical heterogeneity across outcomes. Effects on self-esteem, quality of life, self-efficacy, and psychiatric symptomatology were limited or inconsistent across studies. No studies specifically evaluated interventions focused on physical appearance care. Conclusions: Non-pharmacological interventions appear to produce modest but potentially meaningful reductions in self-stigma among individuals with SMI, particularly when delivered through multicomponent psychosocial approaches that integrate psychoeducation, cognitive restructuring, narrative techniques, and social support. Full article

Inflammatory bowel disease (IBD) poses a significant global health burden with rising incidence, particularly in Asia. This study employed an integrative network pharmacology approach combined with molecular docking to elucidate the therapeutic mechanism of ganoderic acid A (GAA) against IBD. Potential GAA targets were retrieved from pharmacogenomic databases, while IBD-related genes were curated from OMIM and GeneCards databases. Weighted gene co-expression network analysis of IBD transcriptomic datasets (GSE38713, GSE126124) identified disease-associated modules, with the yellow module exhibiting the strongest positive correlation. Functional enrichment analyses demonstrated significant involvement of overlapping targets in lipid metabolism, the inflammatory response, and the mitogen-activated protein kinase (MAPK) signaling cascade pathway. We identified 14 IBD-GAA-ferroptosis-related genes and 54 key module genes. Intersection analysis revealed 5 overlapping targets, including tumor necrosis factor-α(TNF-α), peroxisome proliferators-activated receptor γ (PPARγ), MAPK14, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic α (PIK3CA), and Caspase 3 (CASP3). Molecular docking confirmed high-affinity binding of GAA to these targets, with binding energies ranging from −7.3 to −10 kcal/mol. Crucially, experimental evaluation demonstrated the pivotal role of GAA in alleviating disease pathology. GAA treatment suppressed the significantly elevated levels of TNF-α and p-MAPK14 in the organoids using a cytokine/LPS-induced IBD model. These findings collectively suggest a potential involvement of GAA in pathways associated with ferroptosis regulation, although direct experimental evidence for ferroptosis markers remains to be established. The observed multi-target effects on immune regulation and cellular proliferation/differentiation provide a foundation for further mechanistic investigation. Full article

New copper(II) (C1) and palladium(II) (C2) complexes with S,O-tetradentate ligand (L) derived from thiosalicylic and thiopropionic acids were synthesized. In cell-based assays, (C1) exhibited the most pronounced activity within the tested compound series and was therefore advanced for mechanistic evaluation in 4T1 triple-negative breast cancer cells. (C1) significantly reduced 4T1 cell viability by inducing early and late apoptosis, accompanied by mitochondrial membrane depolarization and enhanced cytochrome C release. Consistently, (C1) increased the Bax/Bcl-2 ratio, promoting a pro-apoptotic shift. In parallel, (C1) triggered autophagy, as evidenced by decreased p62 and LC3B levels, induced G0/G1 cell-cycle arrest, and suppressed proliferative signaling by downregulating Ki67, cyclin D, and phosphorylated AKT. The DNA-binding studies showed moderate to strong affinity, favoring minor groove binding, with higher affinity for (C1) than for (C2). Tryptophan fluorescence quenching indicated a strong interaction with BSA via a predominantly static mechanism, more pronounced for (C1). Molecular docking at the DNA and BSA binding sites corroborated experimental findings and suggested favorable interactions between the complexes and apoptosis-related proteins (CASP3, BAX, and BCL2). The integrated experimental and computational data identify (C1) as a biologically active compound with multimodal biological effects in vitro, supporting further structural optimization and mechanistic investigation. Full article

This study aimed to investigate the selective anticancer activity of the curcumin analog PAC (3,5-Bis-4-hydroxy-3-methoxybenzylidene)-N-methyl-4-piperidone). Normal gingival epithelial cells (GECs), cancerous gingival cells (Ca9-22) and tongue squamous carcinoma cells (CAL27) were exposed to increasing concentrations of PAC (0–10 µM) for 24 h. Cell viability and cytotoxicity were evaluated using MTT and LDH assays, while apoptosis and caspase activation were analyzed by Annexin V/PI staining and flow cytometry. Gene-expression profiling was performed using RT² Profiler PCR arrays. PAC significantly inhibited Ca9-22 and CAL27 cell proliferation in a concentration-dependent manner, with an IC₅₀ value of 5 µM, while exerting no noticeable cytotoxic effects on normal GEC. PAC treatment induced significant early and late apoptosis associated with increased caspase activity in both oral cancer cell lines. Transcriptomic analyses revealed extensive modulation of apoptosis-related genes. In Ca9-22 cells, PAC predominantly suppressed anti-apoptotic and survival-associated genes, including BCL2, BIRC3, BIRC5, XIAP, CFLAR, and NFKB1. In contrast, CAL27 cells exhibited a more pronounced pro-apoptotic transcriptional profile characterized by upregulation of TP53, APAF1, CASP1, BID, and TNF. Gene interaction network analyses further demonstrated that PAC targets highly interconnected apoptotic signaling pathways. Collectively, these findings demonstrate that PAC exerts potent selective anticancer activity against OSCC cells through modulation of intrinsic and extrinsic apoptotic pathways. These results further support the therapeutic potential of PAC as a promising multitarget candidate for oral cancer treatment. Full article

Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by mucosal barrier disruption and dysregulated immune responses. While Intravenous Immunoglobulin (IVIG) is widely used for its immunomodulatory effects in various autoimmune conditions, its specific therapeutic mechanisms and molecular targets in colitis remain to be fully elucidated. Objective: To elucidate the therapeutic mechanisms of IVIG in dextran sodium sulfate (DSS)-induced colitis, with a focus on pyroptosis regulation via the NOD-like receptor (NLR) signaling pathway. Methods: Colitis was induced in mice via DSS administration. IVIG was administered intravenously during disease progression. Colon tissues underwent proteomic profiling, and key targets (GBP5, NLRP3, Pro-Caspase-1, GSDMD) were validated by Western blotting (WB), while interleukin (IL)-1β and IL-18 levels were quantified via ELISA. Results: IVIG significantly attenuated weight loss, Disease Activity Index (DAI) scores, colon shortening, and histopathological damage. Proteomics analysis identified 172 differentially expressed proteins between DSS and DSS + IVIG groups, with pronounced downregulation of GBP5 and NLR pathway components. IVIG suppressed GBP5/NLRP3/CASP1 activation, reduced GSDMD cleavage, and significantly decreased IL-1β production (while showing a decreasing trend for IL-18). Conclusions: IVIG ameliorates colitis by inhibiting the GBP5/NLRP3/CASP1-mediated pyroptosis pathway, highlighting its potential as a targeted therapy for ulcerative colitis. Full article