Search Results (35,336)

Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted by intestinal endocrine L cells that activates the GLP-1 receptor (GLP-1R), leading to glucose-dependent insulin secretion and suppression of glucagon release. In recent years, GLP-1R agonists (GLP-1RAs) have become one of the leading therapeutic options for the treatment of type 2 diabetes mellitus; however, for a long time clinically approved GLP-1RAs were limited to peptide drugs unsuitable for oral administration. The discovery of the “first-in-class” small molecule agonist danuglipron in 2018 demonstrated the feasibility of orally available GLP-1RAs and stimulated the development of numerous danuglipron-like compounds, some of which showed increased efficacy over the prototype. In this study, we report the design and synthesis of novel GLP-1RAs based on a regioisomeric danuglipron scaffold, 1H-benzo[d]imidazole-5-carboxylic acid. A series of 35 compounds was synthesized and evaluated in vitro for cytotoxicity and GLP-1R agonistic activity using a cAMP accumulation assay. A potent lead compound 12r (pEC₅₀ = 7.72, pCC₅₀ < 3.60) was found which is a close structural analog of danuglipron with reduced cytotoxicity and excellent selectivity over two other class B GPCRs, including GCGR and GIPR. Despite decreased potency compared to danuglipron, the obtained results hold promise for further optimization and provide valuable structure–activity relationship insights. Full article

Tumor metastasis is closely associated with coagulation and inflammation, particularly via thrombin–PAR1 signaling. However, the potential of natural polysaccharides such as rhamnan sulfate (RS) to modulate these pathways and suppress metastasis remains unclear. We aimed to investigate the effects of orally administered RS derived from Monostroma nitidum on melanoma metastasis and its underlying mechanisms. Male C57BL/6J mice were orally administered water or RS daily. On day 8, saline or B16 melanoma cells were injected intravenously. Mice were treated for 21 days and divided into four groups (control, RS-only, M + W, and M + RS; n = 5/group). Metastasis and related molecular factors were analyzed in plasma, lung, and aortic tissues. Significant lung and aortic metastases were observed in the M + W group but were markedly suppressed in the M + RS group. RS reduced the expression of inflammatory factors (e.g., IL-6, PAR1), proteases, leukocyte activation markers, complement factors, angiogenic factors, and EMT-related factors. Conversely, thrombin, thrombomodulin, plasmin, TAFIa, and tight junction proteins were increased in RS-treated mice. RS suppresses melanoma metastasis by modulating thrombin–PAR1-mediated inflammation and associated pathways. These findings suggest RS as a potential therapeutic agent, although further mechanistic and clinical studies are required. Full article

Queen bees form the core of honeybee colonies for reproduction, and their quality is the most critical factor affecting their reproductive and productive performance. In apicultural production, queen rearing requires beekeepers to perform manual larval grafting. This is strongly limited by the beekeepers’ eyesight and technical proficiency and has become a bottleneck restricting the development of modern apiculture. To overcome this long-standing technical challenge, we designed beeswax-based tools for queen rearing without grafting larvae for Apis mellifera. The tools consist of three core components: a single-sided hollow beeswax comb foundation, beeswax larval holders and beeswax queen cells with a hole at the bottom. The holders are paired with the hollows of the beeswax comb foundation and the hole of the beeswax queen cells. Following the construction of the comb by honeybees on the hollow foundation, the queen was confined to lay eggs on the single-sided comb. Subsequently, larval holders containing eggs or larvae were pulled out, assembled with beeswax queen cells, embedded in the buckles of queen-rearing frames, and placed into colonies for queen rearing. In order to verify the feasibility of the tools, a paired comparative experiment was conducted using Apis mellifera, with the tools as the treatment group and manual larval grafting as the control group. We evaluated multiple key indicators, including acceptance rate of queen cells, queen cell length at emergence, emergence rate, weight of newly emerged queen, morphological indices (thorax length/width, forewing width, hindwing length, head width), ovariole number and the relative mRNA expression of four queen development-related genes (Vg, Hex110, Hex70b, Jhamt). No significant differences were observed in queen cell acceptance rate and emergence rate between the two groups. However, compared with the control group, queens reared using the tools exhibited significantly greater queen cell length at emergence, higher emergence weight, superior morphological traits, more ovarioles and significantly upregulated expression of all four assayed genes. In conclusion, the tools can be used to rear high-quality Apis mellifera queens effectively with superior phenotypic and molecular traits compared to conventional grafting, which provides efficient and convenient queen-rearing tools for beekeepers. Full article

Chronic diabetic wound remain difficult to heal because persistent inflammation, oxidative stress, and impaired regeneration delay repair, while effective noninvasive options are limited. In this study, graphene-based far-infrared radiation (FIR) therapy was evaluated in a streptozotocin (STZ)-induced diabetic rat full-thickness wound model, and mechanisms were examined in vivo and in vitro. Wound closure was quantified by serial imaging, whereas tissue remodeling and angiogenesis were assessed by H&E and Masson’s trichrome staining and CD34-based analyses. Transcriptomic responses were profiled by RNA sequencing with qRT-PCR validation, immune phenotypes were characterized by immunofluorescence, and high-glucose cell assays were performed. Re-epithelialization, collagen deposition, and neovascularization were quantified histologically. These datasets enabled integrated evaluation of inflammation, oxidative stress, and repair programs over time. Graphene FIR accelerated closure, reaching 83.9% healing by day 14 vs. 66.8% in untreated controls. Treatment was associated with downregulation of Cxcl2/Cxcl3, suppression of M1 polarization with enhanced M2 polarization, and reduced ROS accumulation. Consistently, NF-κB signaling was inhibited, supporting restoration of a pro-regenerative microenvironment. Collectively, graphene FIR represents a promising noninvasive strategy for diabetic wound repair via coordinated immunomodulatory and antioxidant actions. Full article

Oxidative stress is no longer viewed as a random imbalance between reactive oxygen species and antioxidants, but as a failure of an integrated redox network that connects metabolism, immunity, and metal homeostasis. Classical markers such as malondialdehyde and 4-hydroxynonenal define oxidative damage, yet they cannot explain how redox adaptation occurs or fails. Over the past decade, the discovery of regulated cell-death pathways (ferroptosis, cuproptosis) and emerging metabolic signals has revealed a new generation of adaptive redox mediators—including itaconate, nitro-fatty acids, reactive sulfur species and succinate—that act as electrophilic or persulfidating regulators rather than passive by-products of oxidation. This review integrates mechanistic, biochemical and clinical evidence to define how these mediators remodel the nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1, nuclear factor kappa-light-chain-enhancer of activated B cells, and hypoxia-inducible factor 1-alpha axes, coordinate lipid–metal–sulfur cross-talk, and shape vulnerability or resistance to ferroptosis and cuproptosis. By combining deep molecular research with translational perspectives, we propose a unifying framework for predictive redox medicine based on composite biomarker panels and AI-assisted phenotyping. Understanding and quantifying these next-generation mediators will open new avenues for precision nutrition, drug development, and disease prevention—transforming oxidative-stress biology from a descriptive field into an actionable platform for human health. Full article

Prostaglandin E₂ (PGE₂) plays a critical role in regulating uterine endometrial function and supporting embryonic development during early pregnancy in ruminants. However, its precise roles in shaping the uterine microenvironment remain unclear. Herein, 1 mg PGE₂ was infused daily into the uterus of dairy heifers from days 12 to 14 of the estrus cycle. ULF was subsequently collected for integrated proteomic, metabolomic, and targeted lipidomic analyses. In addition, bovine endometrial epithelial cells were used to evaluate the effects of PGE₂ on epithelial adhesion and responsiveness to interferon tau (IFNT). PGE₂ infusion resulted in 909 differentially abundant proteins (DAPs), which are primarily associated with early embryonic development, immune regulation, and cell adhesion. Untargeted metabolomics analysis identified 587 altered metabolites, which were enriched in sphingolipid, arachidonic acid, phenylalanine, and tryptophan metabolism. Proteomic–metabolomic analyses showed that these alterations were primarily associated with early embryonic development, immune regulation, and cell adhesion. Targeted lipidomic analysis showed a global reduction in lipid accumulation, with glycerophospholipid metabolism and choline metabolism most significantly affected. In vitro, PGE₂ reduced epithelial microvilli density, increased osteopontin (OPN) expression, and decreased the expression of junctional proteins (zona occludens-1 (ZO-1), E-cadherin (CDH1), and fibronectin 1 (FN1)). Moreover, PGE₂ enhanced the responsiveness of bEECs to IFNT by interferon alpha/beta receptor 1 (IFNAR1) and IFNAR2, and prostaglandin E receptor 4 (PTGER4) was identified as the primary receptor mediating this response. Collectively, these findings suggest that PGE₂ may modulate lipid metabolism and adhesion-related processes in the endometrium and influence endometrial responsiveness to IFNT, providing insights into molecular mechanisms associated with pregnancy establishment in dairy cows. Full article

Background/Objectives: Epigenetic modifications, particularly DNA methylation, contribute to tumor progression and therapy resistance. Guadecitabine, a hypomethylating agent (HMA), has shown promising clinical activity when combined with carboplatin in preclinical models. We evaluated the combination of guadecitabine with carboplatin as a second-line treatment for extensive-stage small-cell lung cancer (SCLC; NCT03913455), one of the deadliest malignancies. Here, we report methylome changes in peripheral blood mononuclear cells (PBMCs) collected at baseline and during treatment from patients on the trial. Methods: PMBC DNA was analyzed using Infinium HumanMethylationEPIC v1.0 bead chips. Data were processed, and differentially methylated positions (DMPs) were identified and analyzed for pathway enrichment using bioinformatic approaches, and immune deconvolution analyses were conducted to investigate the impact on immune cell composition. Results: Direct comparison of PBMCs between cycle 2 day 5 (C2D5; post-treatment) vs. cycle 1 day 1 (C1D1; pre-treatment) revealed a greater number of hypomethylated DMPs (380 DMPs in C2D5 vs. C1D1 PBMCs; p < 0.05, |β| > 20%). Moreover, when first compared with normal PBMCs from cancer-free controls, the number of hypomethylated DMPs was even greater in C2D5 than in C1D1 (1771 vs. 237 DMPs, respectively; p < 0.05, |β| > 20%). Long interspersed nucleotide elements-1 (LINE-1) were significantly hypomethylated in PBMCs after HMA treatment (C2D5 vs. C1D1). Pathway analysis of hypomethylated DMPs revealed significant alterations in key signaling pathways, including NF-κB, Rho GTPase, and pulmonary fibrosis in C1D1 vs. C2D5. Normal PBMCs to C1D1 PBMCs revealed changes in IL-3 signaling, Fcγ receptor-mediated phagocytosis, and molecular mechanisms of cancer. Deconvolution analysis revealed a greater percentage of monocytes in C1D1 vs. normal PBMCs; after HMA treatment, percentages of monocytes and B cells decreased, while the eosinophil percentage increased in C1D1 vs. C2D5. Conclusions: HMA treatment has a global impact on PBMC methylomes in cancer patients. DNA methylation changes were associated with biological pathways related to PBMC function, and shifts in distinct immune cell populations were observed. Full article

Background/Objectives: T-cell lymphomas are relatively common in veterinary species, yet current diagnostic tools such as PCR-based clonality assays often lack sensitivity and specificity. In humans, we recently developed two related tissue-based diagnostic approaches based on the differential detection of the mutually exclusively expressed TCRbeta1 and 2 (TCRβ1 and 2) constant region proteins, or the corresponding TRBC1 and TRBC2 transcripts. Analogous to the detection of kappa/lambda light chains for the diagnosis of B-cell/plasma cell neoplasms in human clinical practice, our TCRβ1/2 diagnostic assay has the potential to transform veterinary diagnostic workflows. Methods: We identified and confirmed the sequences of the relevant TRBC1 and TRBC2 sequences in both cats and dogs, focusing on the 3′ untranslated region (UTR), where there is the least sequence homology between TRBC1 and TRBC2. To allow us to design appropriate probe sequences, we confirmed a lack of 3′UTR in either species, and we observed limited 3′ untranslated region UTR sequence polymorphism in the cat but not in the dog 3′UTR. We designed BaseScope™ RNA in situ hybridization probes targeting the 3′ UTR to distinguish between TRBC1 and TRBC2 transcripts in formalin-fixed paraffin-embedded tissues. Results: In normal tissues, we found the TRBC2:TRBC1 expression ratio to be similar to the 1.2:1 ratio in humans, between 1:1 and 3:1, skewing towards TRBC2, in both dogs and cats. These findings were corroborated using quantitative reverse transcription PCR. Applying our in situ hybridization probes to cases of T-cell lymphoma in dogs and cats, we demonstrated that an assay for differential expression of TRBC1 and TRBC2 in T-cell populations could identify clonal T-cell populations, as in human diagnostics. If further studies corroborate this proof-of-concept study, TRBC1/2 detection could obviate the need for slow, complex and expensive multiplexed PCR-based (PCR for antigen receptor rearrangements (PARR)) clonality assays. Conclusions: This study provides proof-of-concept data for a novel diagnostic approach that could simplify and substantially improve the accuracy of lymphoma diagnostics in veterinary medicine, by detecting TRBC1/2 transcripts. Full article

Background and Objectives: Accurate assessment of liver fibrosis is essential for treatment decisions in patients with chronic hepatitis B (CHB). Although liver biopsy is considered the reference standard, its invasive nature limits routine use. Serum-based non-invasive fibrosis scores have been proposed as alternatives; however, their diagnostic performance in CHB remains variable. This study aimed to compare multiple serum-based non-invasive fibrosis scores with liver biopsy findings and to evaluate their association with histological activity. Materials and Methods: This retrospective cross-sectional study included 219 adult patients with CHB who underwent liver biopsy with simultaneous laboratory evaluation. Patients with viral co-infections (HIV, HCV, or HDV), metabolic syndrome, diabetes mellitus, hepatic steatosis, or incomplete data were excluded. Non-invasive fibrosis scores—including APRI, FIB-4, AST/ALT ratio (AAR), age–platelet index (API), GGT-to-platelet ratio (GPR), Lok index, modified Forns index, Albumin–Bilirubin (ALBI) score, and red cell distribution width (RDW)-based indices—were calculated using routine laboratory parameters. Histopathological fibrosis staging served as the reference standard. Diagnostic performance was evaluated using receiver operating characteristic (ROC) curve analysis, and areas under the curve (AUC) were compared using the DeLong test. Associations with histological activity index (HAI) were assessed using Spearman correlation. Results: For the prediction of significant fibrosis (≥F2), FIB-4 demonstrated the highest AUC, followed by ALBI and APRI. For advanced fibrosis (≥F3), FIB-4 again showed the highest AUC, followed by APRI and GPR. For significant fibrosis (≥F2), DeLong analysis revealed no statistically significant differences between FIB-4 and the other serum-based scores (p > 0.05). APRI (r = 0.556, p < 0.001) and FIB-4 (r = 0.463, p < 0.001) showed the strongest correlations with HAI. In ROC analysis for moderate-to-severe histological activity (HAI ≥ 4), APRI demonstrated the highest diagnostic accuracy (AUC = 0.677). Conclusions: Serum-based non-invasive fibrosis scores demonstrate comparable but overall modest diagnostic performance for biopsy-confirmed fibrosis in patients with chronic hepatitis B. Indices such as FIB-4 and APRI demonstrated relatively better discrimination and may be considered as screening or rule-out tools in selected clinical contexts. APRI and FIB-4 also show associations with histological activity; however, their clinical application should be interpreted with caution, given their moderate discriminatory capacity. Full article

In this study, we investigated the long-term evolutionary dynamics of human norovirus GII.17[P17] using the RNA-dependent RNA polymerase (RdRp) region and the VP1 capsid gene, integrating phylogenetics, time-scaled inference, phylodynamics, and structure-based analyses. Maximum-likelihood phylogenies of both genomic regions consistently resolved four major clades (Clades 1–4). VP1 patristic-distance distributions indicated higher within-clade diversity in the phylogenetically basal Clades 1 and 3, whereas Clades 2 and 4 showed lower diversity, consistent with recent demographic expansion. Similarity-plot analysis identified pronounced variability in the VP1 P2 domain, while the S and P1 domains remained comparatively conserved, supporting P2 as the primary hotspot of diversification. Bayesian time-scaled analyses estimated the most recent common ancestor around 1993 (VP1) and 2000 (RdRp) and revealed two major lineages (Clade 1/2 and Clade 3/4), with the split between Clades 3 and 4 occurring around 2016–2017. Bayesian skyline plots showed a marked increase in effective population size after 2013, and substitution-rate estimates indicated faster evolution in VP1 than in RdRp, with higher VP1 rates in the Clade 3/4 lineage than in Clade 1/2. Capsid dimer modeling further mapped high-confidence conformational B-cell epitopes and positively selected residues predominantly to the distal surface of P2, with broadly conserved spatial patterns across clades. Compared with the Clade 1 reference (Kawasaki323), Clade 2 accumulated numerous P2 substitutions, whereas Clades 3 and 4 retained fewer changes and remained closer to Clade 1 at the amino-acid level. Together, these results suggest lineage turnover within GII.17[P17] driven by constrained diversification at the P2 surface, potentially contributing to the recent predominance of the Clade 3/4 lineage. Full article

Extracellular vesicles (EVs), as key mediators of intercellular communication, play multifaceted roles in the pathogenesis, treatment, drug resistance, and monitoring of B-cell non-Hodgkin lymphomas (B-NHLs), including diffuse large B-cell lymphoma (DLBCL), Burkitt lymphoma (BL), follicular lymphoma (FL), and mantle cell lymphoma (MCL). EVs derived from lymphoma cells or tumor microenvironment cells carry diverse cargoes such as proteins, microRNAs (miRNAs), and viral oncoproteins, which regulate tumor progression by modulating signaling pathways related to cell proliferation, invasion, apoptosis, autophagy, and immune suppression. In terms of treatment, accumulating evidence suggests that EVs may be associated with the efficacy of classical regimens such as R-CHOP, and they also hold potential as therapeutic targets and drug delivery vehicles for B-NHL. They contribute to drug resistance by altering the expression of key molecules or reshaping the tumor niche. Additionally, EV-derived biomarkers enable non-invasive diagnosis and monitoring of treatment response and prognosis. This review summarizes the latest research progress on the roles of EVs in major B-NHL subtypes, aiming to provide new insights for the development of innovative diagnostic and therapeutic strategies for B-NHL. Full article

Hypoxia, a hallmark of hepatocellular carcinoma (HCC), regulates metabolic reprogramming, tumor progression, and therapy resistance. Although hypoxia-induced glycolytic changes are recognized, it remains unclear how intrinsic tumor aggressiveness influences the magnitude and plasticity of metabolic and transcriptional responses to oxygen deprivation. In this study, we investigated the effects of chronic hypoxia (1% O₂ for 48 h) in spheroids generated from two immortalized (HepG2, Hep3B) and two patient-derived HCC cell lines with distinct aggressiveness (HLC19, HLC21). The metabolic activity, energetic status, proliferation, and expression of hypoxia- and metabolism-related genes were assessed, with oxygen levels monitored to validate experimental conditions. It has resulted that immortalized HCC spheroids displayed similar metabolic and transcriptional responses to hypoxia, with enhanced glycolytic activity but limited phenotypic plasticity. Primary HCC spheroids exhibited aggressiveness-dependent differences. Aggressive HLC19 cells showed a pre-established glycolytic phenotype, stable ATP levels, sustained proliferation, and minimal transcriptional remodeling under hypoxia. Less aggressive HLC21 cells relied on the delayed glycolytic activation and induction of hypoxia-responsive genes to maintain viability. Clustering analyses indicated that metabolic strategies, rather than absolute activity, aligned with tumor aggressiveness. These findings suggest that intrinsic tumor aggressiveness shapes hypoxia-driven metabolic programs in HCC and supports the relevance of patient-derived 3D models for studying metabolic adaptation. Full article

Dental tissue regeneration, particularly alveolar bone and gingival repair, remains a major challenge in regenerative medicine. 3D bioprinting offers patient-specific and anatomically precise constructs, representing an advanced alternative to conventional grafting. In this study, nanohydroxyapatite (nHA), chitosan (CS), and collagen (CoL) were combined to fabricate and characterize 3D bioprinted dental grafts. SEM revealed a highly porous, interconnected architecture favorable for cell infiltration and nutrient exchange. EDS confirmed Ca/P ratios of 2.06 for nHA/CoL and 1.83 for nHA/CS/CoL, both of which are above the stoichiometric 1.67, indicating the presence of additional mineral phases and ion substitutions. FTIR and XRD verified characteristic functional groups and crystalline phases, including B-type HA with carbonate substitution. Mechanical testing showed that pure nHA exhibited the lowest compressive strength, whereas CoL incorporation improved stiffness. The nHA/CS/CoL composite achieved the highest compressive strength, elastic modulus, and toughness, demonstrating superior mechanical resilience. DSC analysis indicated endothermic peaks at 106.49 °C and 351.91 °C, with enthalpy values (264.91 J/g and 15.09 J/g) surpassing those of nHA alone. TGA revealed ~28.8% weight loss across three degradation stages, confirming enhanced thermal stability. In vitro cytocompatibility testing using L929 fibroblasts validated the biocompatibility of the composites. Collectively, the synergy between bioceramics and biopolymers markedly improved both mechanical and thermal performance. These findings position the nHA/CS/CoL scaffold as a promising candidate for clinical applications in dental tissue regeneration. Unlike conventional grafting materials, this study introduces a synergistically optimized nHA/CS/CoL bio-ink formulation specifically designed for extrusion-based 3D bioprinting of patient-specific dental constructs. The core innovation lies in the precise integration of nHA within a dual-polymer matrix (CS/CoL), which bridges the gap between mechanical resilience and biological signaling, achieving a compressive strength that mimics native alveolar bone while maintaining high cytocompatibility. Full article

Melanoma is characterized by a high mutational burden making it an established model for studying tumor neoantigens and developing strategies for personalized immunotherapy. In this study, a reproducible bioinformatics pipeline was developed and implemented for the identification and prioritization of candidate neoantigens derived from non-synonymous somatic mutations in melanoma, using genomic data from the MSK-IMPACT cohort (mel-mskimpact-2020; n = 696) and comparative reference information from TCGA-SKCM. From the somatic mutation annotation file (MAF), 16,311 non-synonymous mutations were filtered, from which 50,480 mutant 8–11-mer peptides were generated using a sliding-window approach centered on the mutated position. Peptide–HLA class I binding affinity was predicted using MHCflurry 2.0 across six representative alleles (HLA-A*02:01, HLA-A*24:02, HLA-B*35:01, HLA-B*39:05, HLA-C*04:01, and HLA-C*07:02). Candidate prioritization was initially based on predicted binding percentile (rank ≤ 2), identifying 12,209 peptide–HLA combinations with high predicted binding affinity. To refine candidate selection, additional computational analyses were incorporated, including proteasomal cleavage prediction using NetChop 3.1 and estimation of T-cell epitope immunogenicity using the Immune Epitope Database (IEDB) immunogenicity predictor. Furthermore, a direct comparison between mutant (MUT) and corresponding wild-type (WT) peptides was performed using Δaffinity and Δrank metrics to evaluate the predicted impact of somatic mutations on HLA binding. The analysis revealed a predominance of peptides associated with the HLA-B locus, particularly the allele HLA-B*35:01, among the interactions with the lowest predicted binding percentiles. Several high-ranking peptide candidates were derived from genes with known roles in melanoma biology, including PLCG2, GATA3, AKT1, PTEN, PTCH1, and SMO. Overall, the integrative computational framework implemented in this study enables the systematic prioritization of candidate neoantigens derived from non-synonymous mutations in melanoma. This pipeline provides a reproducible strategy for exploring tumor neoantigen repertoires and may serve as a foundation for subsequent experimental validation and for studies related to neoantigen-based immunotherapies and immunopeptidomics. Full article

Acidic polysaccharides, valued for their outstanding bioactivity and physicochemical properties, represent a promising strategy for metabolic disease intervention. In this study, three acidic polysaccharide fractions (BRP-1, BRP-2, and BRP-3) were isolated from Brassica rapa L. using membrane filtration and ion-exchange chromatography. BRP-3, notable for its high galacturonic acid content (76.64%), was further purified to yield the homogeneous fraction BRP-3-1 (Mw = 22.3 kDa). Combining GC-MS, FTIR, and NMR analyses, we report for the first time the detailed structure of BRP-3-1—a heteropolysaccharide composed of rhamnose (1.687%), galacturonic acid (75.584%), galactose (14.452%), and arabinose (8.277%)—with a backbone composed with T-α-L-Araf-(1 → 5)-α-L- Araf -(1 → 4)-α-D-GalpA-(1 → 4)-α-D-2-O- GalpA Me-(1 → 4)-α-D-GalpA-(1 → 4)-α-D-GalpA-(1 → 3)-Galp-(1 → 4)-α-D-GalpA, and T-Rhap, T-Galp as well as T-GalpA for branched chain and terminals. In HepG2 insulin-resistant cells, BRP-3-1 demonstrated potent dual regulation of glucose and lipid metabolism—enhancing glucose consumption, lowering total cholesterol, and significantly reducing triglyceride levels in the high-dose group (800 μg/mL), outperforming BRP-2. This work systematically defines the structure of a highly bioactive acidic polysaccharide from B. rapa L. and confirms its metabolic regulatory effects, offering a strong scientific foundation for its application in functional foods and as an adjuvant therapeutic for metabolic disorders. Full article