Search Results (28,139)

Background: Diffuse Large B-cell Lymphoma (DLBCL) is a biologically heterogeneous subtype of non-Hodgkin’s lymphoma (NHL), accounting for 30–40% of cases worldwide. Despite the incorporation of rituximab into standard chemo-immunotherapy regimen, approximately one-third of patients present with relapsed or refractory disease, implicating the need for improved prognostic markers and therapeutic targets. Gene expression profiling successfully classified DLBCL into Germinal Center B-cell-like (GCB) and non-GCB subtypes, which differ in genetic alterations, response to therapy, and clinical outcome. While intrinsic tumor biology has been extensively studied, the contribution of the tumor microenvironment (TME) to disease progression and therapeutic resistance still remains incompletely understood. Methods: In this study, we investigated the mutational landscape of stromal-related genes in DLBCL and evaluated their impact on gene expression, downstream signaling pathways, and tumor progression. Results: A total of 176 DLBCL patients were screened, of which 113 were enrolled based on availability of complete clinical data. The cohort demonstrated male predominance (male:female ratio: 2.1:1), advanced disease stage in 72.6% of patients, and elevated serum lactate dehydrogenase levels in 57.5%. Based on immunohistochemistry, 43.4% cases were classified as GCB-DLBCL and 56.6% as non-GCB DLBCL. Although the International Prognostic Index (IPI) retained prognostic significance for event-free survival (EFS) and overall survival (OS), considerable heterogeneity was observed within similar risk groups. Whole-exome sequencing (WES) uncovered recurrent somatic mutations in key oncogenic and epigenetic regulators, including TNFAIP3, NFIB, NOTCH1, TSC2, EZH2, EP300, KMT2D, and B2M, with subtype-specific distribution. Pathway enrichment analysis implicated role of Notch, Wnt, mTOR, JAK-STAT, TGF-β, and antigen-presentation pathways. Comprehensive WES analysis identified multiple novel mutations in genes associated with the stromal/extracellular matrix with distinct patterns in GCB and non-GCB DLBCL, accompanied by concordant alterations in gene expression profiles, suggesting functional relevance within the TME. Functional validation through primary cell culture demonstrated significantly elevated Th2 (IL-4, IL-6, IL-10) and Th17 (IL-17) cytokines in co-cultures containing both neoplastic cells and stromal components, underscoring the role of TME in DLBCL progression. Conclusions: Taken together, this study provides novel insights into stromal mutational signatures and cytokine-mediated tumor–stroma interactions, offering potential prognostic biomarkers and therapeutic targets for the improved management of DLBCL. Full article

Turnera subulata is traditionally used to treat inflammatory and infectious conditions; however; its biological activities remain incompletely characterized. In this study, aqueous (AETS) and hydroethanolic (HETS) extracts obtained from the aerial parts (leaves, stems, and flowers), as used in traditional infusions, were compared regarding physicochemical composition, redox behavior, cytotoxicity, immunomodulatory, and antimicrobial activities. HETS showed significantly higher phenolic content (2555.96 ± 43.55 mg GAE/100 mL) compared to AETS (1269.54 ± 20.60 mg GAE/100 mL) and exhibited stronger DPPH (83.05 ± 0.05%) and ABTS (85.1 ± 1.5%) radical scavenging activity. In contrast, AETS showed greater antioxidant capacity in the TRAP assay from 50 µg/mL (p < 0.0001). Both extracts displayed dose-dependent pro-oxidant behavior in the deoxyribose/Fenton system. In vitro assays demonstrated that both extracts exhibited dose-dependent cytotoxicity in SH-SY5Y cells, with no significant cytotoxic effects observed at concentrations ≤ 50 µg/mL. HETS significantly increased IL-10 levels (p < 0.05), indicating immunomodulatory activity. In antimicrobial assays, HETS showed selective activity against Staphylococcus aureus, with MIC values ranging from 0.625 to 1.25 mg/mL, while no relevant inhibition was observed against Escherichia coli. No synergistic interaction with vancomycin was detected. Overall, the results indicate that the extraction solvent strongly influences the phenolic enrichment and biological activity. The hydroethanol extract showed the most consistent bioactivity, highlighting its potential for applications as a natural antioxidant, immunomodulatory, and anti-staphylococcal agent. Future studies should focus on compound isolation, mechanistic validation, and evaluation in in vivo models to support potential commercial and therapeutic applications. Full article

The root bark of Morus alba L. is commonly used as a natural antioxidant; however, its active constituents and underlying molecular mechanisms remain unclear. In this study, a bioactivity-guided isolation approach was employed to identify antioxidant substances from the root bark of Morus alba L. and to investigate their protective effects against oxidative damage in HaCaT cells. Using techniques such as silica gel column chromatography and semi-preparative HPLC, combined with NMR and HR-ESI-MS analysis, 22 compounds were isolated and identified from the dichloromethane extract of Morus alba L. root bark, including Diels–Alder adducts, flavonoids, and benzofurans. Among them, compounds 1 and 2 are new compounds, while compounds 12 and 16 were isolated from this plant for the first time. Bioactivity screening revealed that Kuwanon A (compound 17) exhibited significant cytoprotective effects in an H₂O₂-induced HaCaT cell injury model, effectively scavenging intracellular reactive oxygen species (ROS), restoring mitochondrial function, and enhancing the activities of antioxidant enzymes such as SOD and GSH. Further studies indicated that H₂O₂ induced ferroptosis in HaCaT cells, characterized by abnormal Fe²⁺ levels, lipid peroxidation, and elevated levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). Kuwanon A significantly ameliorated these pathological changes. Consistently, ELISA and Astral DIA quantitative proteomics analyses demonstrated that Kuwanon A specifically upregulates the expression of the sulfurtransferase NFS1, thereby promoting the expression of the core antioxidant enzyme GPX4 and the iron storage protein ferritin-H, collectively inhibiting ferroptosis. This study elucidates that Kuwanon A is a key active component responsible for the antioxidant and anti-inflammatory effects of Morus alba L. root bark, and its mechanism is closely associated with regulating the NFS1-mediated ferroptosis defense pathway. Full article

Polysaccharides are important bioactive components of dried tangerine peel, exhibiting antioxidant, anti-inflammatory, and hypoglycemic activities. However, the ability of dried tangerine peel polysaccharides to alleviate gastric injury remains insufficiently understood. Therefore, the structure and alleviation of gastric injury induced by dried tangerine peel polysaccharides were explored in this study. Firstly, DTPP-4 was purified from dried tangerine peel. As shown in the HPLC chromatogram, DTPP-4 is a homogeneous polysaccharide with a mean molecular weight of 1.35 × 10³ kDa. DTPP-4 was mainly composed of L-Rha, L-Ara, D-Gal, and D-GalpA with percentages of 10.56%, 9.15%, 4.83%, and 75.45%, respectively. Methylation and NMR results suggested that DTPP-4 was a pectic polysaccharide with →4)-α-D-GalpA-6-OMe-(1→ and →4)-α-D-GalpA-(1→ as the backbone. The alleviation of gastric injury of dried tangerine peel polysaccharide was evaluated in ethanol-induced acute gastric injury mice. Based on the macroscopic images of gastric tissues and the area of gastric tissue injury in mice, the dried tangerine peel polysaccharide can reduce the mouse gastric lesion area and alleviate gastric tissue pathological damage. Histopathological analysis of H&E and PAS staining revealed that the dried tangerine peel polysaccharide could ameliorate the disordered arrangement and necrosis of epithelial cells, reduce inflammatory cell infiltration, and thus alleviate gastric injury. Dried tangerine peel polysaccharide confers gastroprotection by modulating MPO and PGE2 levels, reducing MDA accumulation, enhancing SOD and CAT antioxidant activities, suppressing IL-1β and TNF-α secretion, and upregulating IL-10 expression. These findings provide a theoretical foundation for subsequent structure–activity relationship investigations and provide empirical support for the subsequent development and practical application of this polysaccharide. Full article

Background: Colorectal cancer is a common malignancy and 5-fluorouracil (FU) remains a mainstay of chemotherapy despite its toxicity. As an important part of comprehensive tumor treatment, dual-protein (DP) nutritional intervention is attracting more and more attention. Methods: This study preliminarily evaluated the regulatory effects of DP intervention on colorectal cells of CT26 tumor-bearing mice, examining the dosage and administration methods of DP, as well as the anti-tumor effects of FU alone or in combination with DP. Results: The results showed that low- and medium-dose DP numerically increased spleen index and showed trends toward alleviating FU-induced thymic atrophy, splenic damage, nephrotoxicity, and myocardial injury. It also partly mitigated muscle wasting, prevented FU-induced shortening of the colorectal tract, and reduced intestinal injury. In addition, DP was associated with increased lymphocyte, monocyte, and platelet counts and decreased granulocytes, suggesting possible alleviation of chemotherapy-induced bone marrow suppression and a potential effect on hematopoietic function. Flow cytometry results indicated possible effects of DP on CD4⁺ T and CD8⁺ T cell proliferation or apoptosis, modulation of effector and memory phenotypes, reduced splenic neutrophil levels, balanced B cell function, and maintained natural killer cell activity. In addition, DP intervention also showed trends toward regulating hepatic lipid metabolism and partially alleviating FU-induced dyslipidemia and muscle damage. In addition, DP and FU could increase IL-2, IL-10, GM-CSF and IFN-γ and decrease IL-6 and TNF-α. Conclusion: In conclusion, a moderate dose (0.67 g/kg) of DP had the most favorable trends, and the pre-intervention mode was more effective. This study also provided exploratory data on the potential of DP in reducing chemotherapy-related toxicity. These findings will provide preliminary scientific support for nutritional therapy in colorectal cancer patients, as well as for the research, development, and application of dual-protein foods for special medical purposes. Full article

With colorectal cancer (CRC) accounting for over 1.9 million new cases and 930,000 deaths globally in 2020, there is a critical need for innovative indicators to forecast disease advancement and therapeutic outcomes. The gut microbiome has emerged as a fertile area for discovering such diagnostic and prognostic signals. This narrative review collected current evidence on intestinal microorganisms and their metabolic products as candidate markers for CRC control. Intestinal communities influence malignancy through diverse mechanisms, including metabolic shifts, immune modulation, inflammation, proliferation/apoptosis regulation, genotoxicity, and mucosal barrier disruption. Pathogenic species, such as Fusobacterium nucleatum and enterotoxigenic Bacteroides fragilis, facilitate tumorigenesis via FadA-mediated signaling and Th17/IL-17 responses. In contrast, beneficial taxa like Faecalibacterium prausnitzii and Akkermansia muciniphila provide protective effects through short chain fatty acid production. Macrophage phenotype physiological equilibrium is altered and inflammatory status fluctuates under the former. Metabolically, hydrogen sulfide damages mitochondrial DNA and secondary bile acids stimulate cellular proliferation. While 16S rRNA sequencing and shotgun metagenomics are established detection strategies, innovative platforms like organoids and gene arrays remain in the exploratory stage. Clinical data indicates that F. nucleatum aligns with advanced tumor stage, and its combined detection with colibactin-producing E. coli achieves high sensitivity for early-stage screening. Additionally, A. muciniphila levels can anticipate the efficacy of PD-1 blockade immunotherapy. Microbiota-derived tools represent a transformative direction in oncology. Future research must focus on standardizing protocols and validating multi-marker panels to enhance clinical translation. Full article

Gelatin methacrylate (GelMA) hydrogels are promising carriers for bioactive agents like curcumin (Cur) and adenosine diphosphate (ADP) in wound healing. However, existing GelMA-based systems fail to achieve both rapid hemostasis and sustained anti-inflammatory effects. In this study, we developed a Cur/ADP GelMA hydrogel, and evaluated its anti-inflammatory, regenerative, hemostatic, and biocompatible properties. Proton nuclear magnetic resonance (¹H-NMR) analysis showed that a 65% degree of substitution of GelMA is optimal for wound dressings. Scanning electron microscopy revealed a uniform pore size, aiding inflammatory exudate removal. The Cur/ADP GelMA hydrogel exhibited strong adhesion, stability, and antibacterial activity, reducing E. coli and S. aureus proliferation by 85% and 72%, respectively. Hemostatic effects were observed, with blood loss reduced to 238 ± 23 mg compared to 559 ± 18 mg in the untreated group. The ELISA results showed reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and increased IL-10. In vivo studies demonstrated 98% wound closure by day 14, enhanced granulation tissue formation, and a 70% thicker epidermis compared to controls. Mechanistically, ADP accelerates platelet activation and clot formation, while Cur modulates the inflammatory microenvironment, enabling synergistic hemostasis and immune regulation, thus promoting accelerated wound healing. Full article

Peptide therapeutics have emerged as a versatile class of biomolecules bridging the gap between small-molecule drugs and large biologics. Advantages of such molecules include high target specificity, potent bioactivity and reduced off-target toxicity. Despite these, broader clinical translation remains constrained by inherent limitations like poor metabolic stability, rapid renal clearance, limited membrane permeability and scalable synthesis. This review aims to systematically integrate advances in peptide science across natural discovery, synthetic methodologies, structural engineering, and translational delivery systems, while identifying critical research gaps hindering clinical adoption. We highlight diverse natural sources of bioactive peptides, including plant- (lunasin), animal- (Val-Pro-Pro (VPP) and Ile-Pro-Pro (IPP)), microbial- (nisin and cyclosporine), marine- (dolastatins) and venom-derived (chlorotoxin and ω-conotoxin MVIIA (ziconotide)) agents. Advances in solid-phase peptide synthesis (SPPS), green chemistry, and catalytic strategies are discussed alongside emerging in silico approaches, including artificial intelligence-driven sequence design and molecular modeling. Structural modifications such as cyclization, hydrocarbon stapling, PEGylation, and lipidation are critically evaluated for their role in enhancing pharmacokinetic and pharmacodynamic properties. Furthermore, nanoformulation strategies, including self-assembling peptides and cell-penetrating systems, are examined for their potential to overcome biological barriers. Importantly, this review identifies key unresolved challenges, including the lack of predictive models for peptide delivery systems, safety concerns associated with long-term modifications, and limited in vivo validation of naturally derived peptides. Addressing these gaps through integrated computational and experimental approaches will be essential for advancing next-generation peptide therapeutics. Collectively, this work provides a comprehensive framework for the rational design and translation of peptide-based precision medicines. Full article

SIRT2 (Sirtuin 2) is an NAD+-dependent deacetylase that exerts crucial regulatory effects on immune homeostasis and macrophage activation. While chronic cold exposure is a known predisposing factor for pulmonary dysfunction, the precise mechanisms by which SIRT2 potentially modulates lung macrophage polarization under cold stress remains poorly understood. In this study, we evaluated the protective capacity of SIRT2 using both wild-type (WT) and Sirt2-knockout (Sirt2−/−) murine models subjected to chronic cold exposure (4 °C for 3 h daily over 21 days). Our results demonstrated that Sirt2 deficiency significantly exacerbated cold-induced pulmonary histopathological damage and increased the secretion of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) (p < 0.05). Furthermore, chronic cold stress triggered a macrophage-centered inflammatory response, a process wherein SIRT2 was found to curtail M1 pro-inflammatory polarization. To further investigate these mechanisms, in vitro experiments were conducted using the mouse alveolar macrophage cell line MH-S. While LPS was utilized as a canonical inflammatory stimulus to mimic the injury environment, SIRT2 overexpression was found to reverse the LPS-induced increase in M1 markers and attenuate inflammatory cytokine secretion. These findings suggest that SIRT2 maintains intracellular homeostasis by modulating macrophage plasticity and plays a protective role in the development of chronic cold stimulus-induced lung injury. Consequently, SIRT2 activation may represent a potential therapeutic pathway for the treatment of environment-related respiratory diseases. Full article

Background: Rotenone is a widely used environmental pesticide, and epidemiological studies suggest that exposure is associated with an increased risk of Parkinson’s disease (PD); however, the molecular toxicological basis of this association remains incompletely defined. Ferroptosis is an iron-dependent, lipid peroxidation-driven form of regulated cell death that is relevant to PD and other neurodegenerative disorders. In this study, we provide disease-contextual functional evidence linking ferroptosis to rotenone-induced PD-like neurotoxicity. Methods: We combined network toxicology, human PD substantia nigra transcriptomic analysis using GSE7621, and SH-SY5Y cell-based validation. Rotenone-associated targets were predicted and analyzed for ferroptosis-related enrichment, PD transcriptomic signatures were used for disease-contextual candidate prioritization, and selected findings were validated using qPCR, CCK-8, Western blotting, C11-BODIPY lipid peroxidation staining, and transmission electron microscopy. Results: By further integrating a human PD substantia nigra transcriptomic dataset (GSE7621), we prioritized an 11-gene, PD-contextualized ferroptosis-associated candidate module (LIPF, FAM170A, MCHR1, IL17A, MYB, GFAP, ARMC3, GKN1, GATA3, IL17F, and TEKT1). In SH-SY5Y cells, rotenone exposure consistently upregulated this candidate transcriptional module, and this induction was broadly attenuated by the ferroptosis inhibitor ferrostatin-1 (Fer-1). In parallel, orthogonal functional assays supported an iron- and lipid peroxidation-driven injury state under rotenone exposure that was suppressible by ferroptosis inhibition and iron chelation. Finally, we further performed an exploratory drug–gene association screen to prioritize clinically available candidates, and a limited qPCR check suggested that several selected compounds partially attenuated representative hub-gene induction under rotenone exposure. Conclusions: Collectively, these findings provide disease-contextual and experimentally supported evidence linking rotenone exposure to ferroptosis-associated neurotoxicity, and identify a ferroptosis-responsive transcriptional module for future hypothesis-driven mechanistic investigation. Full article

Lignocellulosic agricultural residues are abundant yet underutilized despite their potential for sustainable bioconversion. This study evaluated spent mushroom substrate (SMS) from Pleurotus ostreatus cultivation and roots of leafy vegetables (RLV) as alternative substrates for Pleurotus production, using wheat straw as a control. Two species, P. ostreatus and P. citrinopileatus, were cultivated on different SMS/RLV ratios and the immunomodulatory potential of harvested mushrooms was assessed. Specifically, protein (PE-D-P3 < 3 kDa) and carbohydrate (CE-D) fractions obtained after in vitro digestion were applied to LPS-challenged THP-1 cells and immune-related gene expression was analyzed by qPCR. Both species significantly modulated immune responses. The PE-D-P3 showed a more pronounced immunomodulatory effect, significantly downregulating IL1B, IL6 and TNF, whereas the CE-D reduced only TNF expression. Substrate composition influenced bioactivity: PE-D-P3 from SMS 80-RLV 20% resulted in the greatest reduction in IL1B, IL6 and TNF, while CE-D from SMS 60-RLV 40% reduced IL1B and CXCL8. These findings provide insights that both fungal species and substrate composition influence immunomodulatory compound production. Valorizing lignocellulosic residues through optimized mushroom cultivation represents a sustainable strategy for producing functional ingredients with applications in human and animal health, particularly for preventing inflammation-related disorders. Full article

Bronchopulmonary dysplasia (BPD) remains a major complication of extreme prematurity, driven in part by persistent inflammation. Interleukin (IL)-1–mediated signaling plays a central role in sustaining lung injury, making IL-1 blockade a potential therapeutic target. Evidence on the use of anakinra, a recombinant IL-1 receptor antagonist, in neonatal BPD is still limited. We report the case of a female preterm infant (28⁺² weeks’ gestation, birth weight 800 g, −1.41 zs) affected by BPD requiring prolonged respiratory support. Due to persistent respiratory failure despite standard therapies, off-label treatment with subcutaneous anakinra (5 mg/kg twice daily) was initiated at 150 days of life. Clinical respiratory parameters and exploratory salivary inflammatory biomarkers (IL-6 and soluble urokinase plasminogen activator receptor, suPAR) were longitudinally monitored. Following anakinra initiation, the patient showed a gradual improvement in respiratory parameters, with reduction in oxygen requirement, mean airway pressure, and improved gas exchange. Respiratory support was gradually de-escalated from nasal intermittent positive pressure ventilation to continuous positive airway pressure and subsequently to high-flow nasal cannula. Salivary suPAR levels demonstrated a decreasing trend, while IL-6 showed transient fluctuations, partly associated with intercurrent infections. Treatment was generally well tolerated during the observation period. The infant was discharged on minimal respiratory support, with continued improvement during follow-up. This case suggests a possible role of IL-1 blockade in the modulation of persistent inflammation in BPD with a refractory clinical course, although the observed clinical course may also reflect the natural evolution of the disease. Longitudinal salivary biomarkers may represent a feasible, exploratory, non-invasive approach to describe inflammatory dynamics over time. Larger prospective studies are needed to evaluate the efficacy, safety, and optimal treatment protocols of anakinra. Full article

Background: Treatment-resistant depression (TRD) represents a major clinical challenge and is increasingly associated with persistent neuroinflammatory processes. Evidence suggests that dysregulation of the immune system, particularly the imbalance between pro-inflammatory and anti-inflammatory cytokines, contributes to poor therapeutic response. In this context, interleukin-10 (IL-10) has emerged as a key mediator in regulating the inflammatory response. Objective: To systematically analyze the evidence on neuroimmune dysregulation in depression, with an emphasis on TRD, and to evaluate the potential role of IL-10 as a biomarker and modulator of therapeutic response. Methods: A systematic review was conducted in accordance with PRISMA guidelines. Fourteen studies were included, comprising randomized clinical trials, longitudinal studies, a prospective cohort study, and exploratory designs. Methodological quality was assessed using the RoB 2 tool and complementary approaches. Data were integrated through a qualitative analysis focused on inflammatory biomarkers and clinical outcomes. Results: The studies consistently showed an association between elevated levels of pro-inflammatory cytokines, such as IL-6 and TNF-α, and the severity of depressive symptoms, as well as reduced response to conventional treatments. Immunomodulatory interventions, including ketamine, pentoxifylline, and minocycline, were associated with clinical improvement, particularly in patients with elevated baseline inflammation. IL-10 appears to be involved in counter-regulatory neuroimmune processes associated with inflammatory balance. Conclusions: Neuroinflammation plays a central role in TRD. IL-10 may serve as a relevant biomarker and a potential target for personalized therapeutic strategies informed by immune profiles, through modulation of neuroinflammatory pathways. Full article

Chronic wound management remains a significant clinical challenge, requiring adaptive therapeutic approaches to achieve wound closure that nonetheless frequently prove fruitless. Balancing the initial pro-inflammatory response with debris removal and tissue rebuilding remains elusive in most cases, leading to pain, drastic quality-of-life deterioration, and, eventually, amputation. Meanwhile, patient adherence is an overarching theme. Furthermore, non-surgical alternatives that effectively promote tissue rebuilding are essential for patients seeking to avoid further invasive procedures. We report a patient with a recalcitrant ulcer managed using human amniotic membrane dressing (hAM-pe) and a bovine collagen matrix (BCM) in spatially distinct areas as an intra-patient control. Methodology included clinical monitoring and ad hoc molecular and histological analyses to assess inflammatory markers and tissue architecture. Following 59 days of observation, the superior evolution of the hAM-pe-treated zone led to the clinical decision to extend hAM-pe treatment over the adjacent BCM area, resulting in total wound closure. The hAM-pe-treated site demonstrated accelerated closure and clinical resolution of inflammation without the presence of a granulomatous response. Molecular analysis revealed downregulated pro-inflammatory mediators (IL-1β, TNF-α, CXCL-10) and upregulated markers associated with angiogenesis (VEGF, CD34) and tissue repair (Arginase-1). In this case, the non-surgical hAM-pe treatment was associated with a favorable healing trajectory, characterized by superior inflammation resolution and enhanced tissue organization (collagen type I/III maturation). While these descriptive findings suggest the potential advantages of amniotic membrane dressings in promoting advanced tissue repair, they remain limited to this individual observation. Further research in larger cohorts is required to validate these mechanisms. Full article

Background: To examine the antioxidant and anti-inflammatory effects of sitagliptin in restoring the intestinal mucosal barrier in rats with colitis induced by dextran sulfate sodium (DSS). Methods: Male Sprague-Dawley rats were administered 5% DSS in their drinking water to induce colitis. Sitagliptin was administered intragastrically at a dose of 15 mg/kg/day for a duration of eight days. Changes in the colon tissue were histologically examined, and the disease activity index (DAI) score was measured. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase were evaluated. Gene expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, tight junction proteins occludin and ZO-1 was assessed. Levels of SGOT, SGPT, and serum iron were also measured. Results: Sitagliptin diminished DAI and histological index scores, as well as MDA levels, while augmenting SOD, GPx, and catalase levels over an eight-day period. Based on proinflammatory cytokines, sitagliptin reduced colon inflammation. Compared to the untreated DSS group, sitagliptin increased serum iron and lowered SGOT and SGPT. Conclusions: The present results indicate that administering sitagliptin orally for a week could aid in the recovery from DSS-induced colitis by reducing oxidative stress and pro-inflammatory cytokines. Additional studies are required to make this applicable for patients suffering from colitis. Full article