Experimental and therapeutic medicine最新文献

{"title":"Fatty acid-activated proton transporter SR4 prevents hepatic steatosis and metabolic alterations in diabetic mice by improving mitochondria function, energy balance and oxidative stress.","authors":"James Figarola, Jyotsana Singhal, Sharad Singhal","doi":"10.3892/etm.2026.13190","DOIUrl":"10.3892/etm.2026.13190","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) is a growing global health crisis, largely driven by rising obesity rates. Untreated T2D leads to severe complications such as cardiovascular disease, nephropathy, retinopathy, neuropathy and hepatic dysfunction. Current therapies primarily manage hyperglycemia but often fail to address core pathophysiological drivers such as insulin resistance and obesity. This highlights an urgent need for novel therapeutics with distinct mechanisms, particularly those targeting energy metabolism and insulin sensitivity, to improve long-term T2D outcomes. Modulating mitochondrial respiration through mild uncoupling has emerged as a promising strategy to promote negative energy balance. SR4, a small-molecule mitochondrial uncoupler, represents a novel class of fatty acid-activated proton transporters. In the present study, the metabolic effects of oral SR4 administration were investigated in male <i>db/db</i> mice, a model of T2D. SR4 significantly reduced body weight gain and improved body composition by selectively decreasing fat mass without affecting lean mass. Indirect calorimetry demonstrated that SR4 treatment increased oxygen consumption and total energy expenditure, independent of food intake. Importantly, SR4 notably improved glycemic control, reduced insulin resistance and prevented dyslipidemia, hepatic steatosis and liver injury. Mechanistically, SR4 activated hepatic AMPK, enhanced mitochondrial respiration and mitigated oxidative stress. Liver transcriptomic profiling further demonstrated broad metabolic reprogramming, including downregulation of lipogenesis and PPARγ signaling, concurrently with the upregulation of genes involved in energy metabolism and antioxidant defense. Collectively, these findings demonstrated that SR4 ameliorates multiple aspects of metabolic dysfunction in an obese T2D mouse model by targeting key pathways in energy regulation and lipid metabolism. The present results provided additional mechanistic insights into the effects of mitochondrial uncouplers in the liver and support further investigation of SR4 and related fatty acid anion transporters as a novel therapeutic class for metabolic diseases.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"195"},"PeriodicalIF":2.3,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148201846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of vitamin D receptor gene variants on psoriasis vulgaris susceptibility and clinical phenotype in a Greek population.","authors":"Polytimi Sidiropoulou, Martha Katsarou, Maria Papasavva, Annia Tsolakou, Akylas Fotiadis, Demetrios A Spandidos, Natalia Rompoti, Irene Stefanaki, Alexander J Stratigos, Nikolaos Drakoulis, Electra Nicolaidou","doi":"10.3892/etm.2026.13188","DOIUrl":"10.3892/etm.2026.13188","url":null,"abstract":"<p><p>Psoriasis vulgaris (PsV) is a complex immune-mediated disease with a polygenic component. Common variants in the vitamin D receptor (VDR) gene have been explored in the context of psoriasis, but findings remain inconsistent and data from the Greek population are scarce. Thus, the present study aimed to investigate the association of the VDR FokI (rs2228570), BsmI (rs1544410) and TaqI (rs731236) single-nucleotide polymorphisms (SNPs) with PsV susceptibility and clinical phenotype in a Caucasian Greek cohort. In this observational cross-sectional study, 203 patients with chronic plaque psoriasis and 812 age-, sex- and ethnically-matched controls of Greek origin were genotyped for the selected VDR SNPs using real-time PCR (melting curve analysis) and SNP-based statistical comparisons were performed. Case-control analyses exhibited a significant association between the BsmI variant and PsV susceptibility under the recessive and allelic models, with the A allele (A vs. G; OR: 0.765; 95% CI: 0.614-0.953; adjusted P=0.032) and AA genotype (AA vs. GA + GG; OR: 0.577; 95% CI: 0.386-0.861; adjusted P=0.028) conferring a protective effect. No impact on PsV risk was observed for FokI or TaqI. Intra-patient subgroup analyses based on clinical traits indicated phenotype-specific contributions: FokI was associated with early-onset and familial disease, TaqI with psoriatic arthritis and both BsmI and TaqI with nail involvement. To the best of our knowledge, this study provides the first evidence that VDR genetic variation may influence PsV susceptibility and clinical expression in the Greek population. The VDR locus could thus serve as a potential biomarker for tailored risk stratification and clinical profiling in PsV. Further large-scale studies integrating genotypic and phenotypic data, especially among Caucasians, are required to validate these findings.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"193"},"PeriodicalIF":2.3,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphological analysis of bronchoalveolar lavage fluid in diagnosing pulmonary aspergilloma in a patient with rheumatoid arthritis: A case report.","authors":"Yuli Zhou, Yuyi Lai, Fuxian Zhou, Xinxin Wang, Xiao He, Juan Jin, Ruikai Zhang","doi":"10.3892/etm.2026.13186","DOIUrl":"10.3892/etm.2026.13186","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder that primarily affects the joints and may be associated with systemic complications. Patients with RA have an increased susceptibility to opportunistic infections, attributable to inherent immune dysregulation as well as immunosuppressive therapies, including tocilizumab, particularly among those with comorbidities or high disease activity. Notably, the use of tumor necrosis factor inhibitors, such as adalimumab and etanercept, has been associated with a higher incidence of invasive pulmonary aspergillosis and chronic pulmonary aspergillosis. The present study reports a rare case of pulmonary aspergilloma in a 75-year-old female RA patient with prior tuberculosis and long-term tocilizumab use. The patient was diagnosed via bronchoalveolar lavage fluid morphology, fungal culture, <i>Aspergillus</i> galactomannan assay, metagenomic next-generation sequencing and pathology, and the patient achieved symptom resolution and improved imaging after 6 months of treatment with voriconazole. These findings underscore the need for vigilant monitoring and individualized management strategies in this patient population.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"191"},"PeriodicalIF":2.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13218273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intravenous leiomyomatosis of the uterus: A case report and literature review.","authors":"Yuzhen Zhao, Fei Tian","doi":"10.3892/etm.2026.13183","DOIUrl":"10.3892/etm.2026.13183","url":null,"abstract":"<p><p>Intravenous leiomyomatosis (IVL) is a rare benign ovarian tumor that predominantly affects women of reproductive and perimenopausal age, and is often accompanied by uterine fibroids. Patients typically present with symptoms such as menorrhagia, anemia, dysmenorrhea, abdominal pain or a palpable abdominal mass. In its early stages, the clinical manifestations of this disease are highly nonspecific and lack typical features, leading to a high rate of underdiagnosis or misdiagnosis in clinical practice. IVL is classified as a borderline tumor due to its histologically benign characteristics but biologically malignant behaviors, such as vascular invasion and distant spread. When the lesion extends to involve the inferior vena cava or even the heart, recurrent syncope may become the predominant clinical manifestation. With disease progression, sudden cardiac arrest of a fatal type may occur. Surgical resection remains the primary treatment for this condition. Given its high recurrence rate, post-operative follow-up should be conducted in a manner similar to that for malignant tumors, with regular imaging surveillance. To enhance clinical awareness of IVL, the present study describes a case of IVL in a patient whose chief complaint was increased menstrual flow, an atypical presentation. By reviewing the current case, practical insights may be provided into the diagnosis and management of IVL.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"190"},"PeriodicalIF":2.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D-Printed prosthesis for recurrent femoral metastasis with periprosthetic infection: A case report.","authors":"Jiangbi Li, Yangjie Zhang, Jianping Kang, Changping Tian, Suolin Chen, Ya Ning, Haixia Li, Yanbin Xiao","doi":"10.3892/etm.2026.13185","DOIUrl":"10.3892/etm.2026.13185","url":null,"abstract":"<p><p>3D-printed prosthesis replacement is increasingly applied for reconstruction following resection of malignant bone tumors. However, the management of postoperative tumor recurrence with periprosthetic infection following surgery remains challenging, as clinical manifestations and imaging features can be obscured by or mimic tumor recurrence, periprosthetic biofilms render conventional antibiotics ineffective and large segmental bone defects limit reconstructive options. The present study reports the case of a 53-year-old female patient with cervical cancer who developed femoral metastasis and tumor recurrence with periprosthetic infection. A customized anatomically matched femoral prosthesis was designed using 3D printing technology. The patient underwent tumor resection, debridement and implantation of the custom prosthesis, followed by prolonged antibiotic therapy. The infection was effectively controlled and limb salvage was achieved. At 1 year postoperative follow-up, the patient was able to ambulate without assistance and reported no notable pain. Personalized 3D-printed prosthesis combined with appropriate antibiotic therapy may offer an effective treatment option for recurrent bone tumors complicated by infection and large segmental bone defects.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"189"},"PeriodicalIF":2.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148140326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycolytic reprogramming in host response to <i>Borrelia burgdorferi</i>: A gene signature revealed by integrative bioinformatics analysis and machine learning.","authors":"Yan Dong, Yantong Chen, Yanshuang Luo, Meng Liu, Chao Song, Xuesong Chen, Fusong Yang, Qingyi Luo, Guozhong Zhou","doi":"10.3892/etm.2026.13182","DOIUrl":"10.3892/etm.2026.13182","url":null,"abstract":"<p><p>Lyme disease (LD), a multifaceted condition caused by <i>Borrelia burgdorferi</i> (Bb), remains poorly understood, particularly regarding metabolic pathways. This study aimed to evaluate the role of glycolysis-related genes (GRGs) in LD pathogenesis and identify key genes and mechanisms relevant to diagnosis and therapy. Differentially expressed GRGs were identified and further analyzed by correlation analysis and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Key genes were screened using least absolute shrinkage and selection operator (LASSO) and support vector machine-recursive feature elimination, followed by gene set enrichment analysis, gene set variation analysis and immune infiltration analysis using CIBERSORT. Diagnostic value was assessed by receiver operating characteristic and nomogram analyses, and a competing endogenous RNA network and protein-drug interaction predictions were constructed. The expression of key genes was further validated by reverse transcription-quantitative PCR (RT-qPCR) in Bb-infected THP-1 cells, and glucose and lactate concentrations in the culture supernatants were measured using commercial colorimetric assay kits. A total of 63 differentially expressed GRGs were identified. Of note, two key genes [lactate dehydrogenase A (LDHA) and thioredoxin (TXN)] exhibited a strong diagnostic performance. Immune infiltration analysis revealed that these genes were associated with regulatory T cells (r=0.33, P=0.05), gamma delta T cells (r=-0.34, P=0.042), CD4 memory resting T cells (r=-0.4, P=0.016) and monocytes (r=-0.36, P=0.03). The potential glycolysis-targeting drugs were predicted. RT-qPCR analysis revealed increased LDHA and TXN expression in Bb-infected THP-1 cells. In addition, Bb stimulation reduced extracellular glucose levels and increased lactate accumulation in culture supernatants. Overall, this integrative analysis revealed notable alterations in glycolytic genes during Bb infection, suggesting that dysregulation of glycolysis contributes to LD immunopathology. The identified key genes (LDHA and TXN) may serve as infection-related transcriptional response markers, offering insights into LD mechanisms and potential precision-based strategies.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"187"},"PeriodicalIF":2.3,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148038723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic etiology and phenotypic characteristics of fetuses with 11q deletion syndrome (11q23.3-q25).","authors":"Tong Zhang, Xiaoyi Cong, Zhenming Li, Xianzhen Cao, Liang Hu, Xiaojin Luo, Yanan Liu, Weiqiang Liu, Fengxiang Wei","doi":"10.3892/etm.2026.13180","DOIUrl":"10.3892/etm.2026.13180","url":null,"abstract":"<p><p>The 11q deletion (11q-) syndrome is a rare consecutive polygenic deletion disorder. Characterization of the clinical features, genetic etiology and diagnostic strategies associated with 11q deletion syndrome in the prenatal setting is important to understand this syndrome in its entirety. A retrospective review at Longgang District Maternity & Child Healthcare Hospital of Shenzhen City (Shenzhen, China) involving four fetuses diagnosed with 11q- syndrome was conducted to examine the clinical features of this syndrome. The cases were identified through prenatal screening, including maternal serum biochemistry, non-invasive prenatal screening (NIPS), chromosomal microarray analysis (CMA) and karyotyping. Pregnant women with high-risk results from NIPS or prenatal serological screening received early interventional prenatal diagnosis and genetic counseling. Of the two cases that showed a high-risk of 11q- by NIPS, invasive diagnostic procedures confirmed the presence of large terminal deletions on chromosome 11q, encompassing telomeric regions. CMA identified the deletions while karyotyping revealed underlying structural rearrangements, including balanced translocations in both cases. Prenatal ultrasound identified cardiac anomalies, such as ventricular septal defects and truncus arteriosus. The variability and incomplete penetrance of these malformations suggest the influence of polygenic (e.g., modifier genes, genetic background, copy number variations), epigenetic (e.g., DNA methylation, histone modification) and environmental factors (e.g., diet, lifestyle, exposure to toxins). The results demonstrated that the phenotypic expression of 11q- syndrome varies according to the size and gene content of the deleted region. The integration of CMA and karyotyping improves diagnostic accuracy and elucidates the origin of chromosomal alterations. In the single case present in the current study that involved a parental chromosomal translocation, karyotyping was essential for determining the risk of recurrence. These findings contribute to a more precise understanding of genotype-phenotype associations and support the provision of informed prenatal counseling and the clinical management of 11q- syndrome.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"185"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13203314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148044962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TPX2 as a prognostic biomarker and potential therapeutic target for malignant melanoma proliferation and metastasis.","authors":"Fuqi Li, Ronghui Yang, Zhixian Wu","doi":"10.3892/etm.2026.13177","DOIUrl":"10.3892/etm.2026.13177","url":null,"abstract":"<p><p>Malignant melanoma is an aggressive skin cancer with increasing incidence and poor prognosis after metastasis. Identifying key molecular drivers of melanoma progression is critical for developing novel therapeutic strategies. Therefore, in the present study, differential gene expression analysis was conducted on GSE98394 and The Cancer Genome Atlas-skin cutaneous melanoma datasets using 'limma' package and Gene Expression Profiling Interactive Analysis 2. Consistently dysregulated genes were intersected and subjected to Kaplan-Meier survival and Cox regression analyses. Functional assays, including reverse transcription-quantitative PCR, western blotting, MTT proliferation assay, wound healing, Transwell migration and small interfering (si)RNA-mediated targeting protein for Xklp2 (TPX2) knockdown assays, were performed in A375 and C32 melanoma cells and PIG1 melanocytes. Intersection of the two datasets revealed eight upregulated and five downregulated genes, and high TPX2 expression was significantly associated with short overall survival. TPX2 mRNA and protein levels were markedly higher in A375 cells than in PIG1 controls. <i>TPX2</i> silencing via siRNA reduced aurora kinase A mRNA and protein levels, inhibited cell proliferation and impaired cell migration in wound healing and Transwell assays. Overall, the integrated bioinformatics and experimental analyses identified <i>TPX2</i> as a potent oncogene promoting cell proliferation and migration, at least in part, via upregulation of aurora kinase A in melanoma. In conclusion, TPX2 may constitute a potential prognostic biomarker and therapeutic target for metastatic melanoma.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"182"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148037728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis.","authors":"Shaodong Zhong, Heng Zhang, Jin Huang","doi":"10.3892/etm.2026.13179","DOIUrl":"10.3892/etm.2026.13179","url":null,"abstract":"<p><p>Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, with malignant metastasis being a major determinant of patient prognosis. The metastatic process involves a number of phenotypic alterations, including enhanced invasive and migratory capacities. The growing availability of unbiased transcriptomic data has facilitated the identification of metastasis-associated molecular biomarkers and has enabled the exploration of their underlying mechanisms, with the aim of identifying novel therapeutic targets. In the present study, differential expression analysis was performed using The Cancer Genome Atlas Stomach Adenocarcinoma dataset to identify genes associated with malignant metastasis in GC. Prognostic signature genes were subsequently identified using Least Absolute Shrinkage and Selection Operator and Cox regression analyses. Western blotting, wound healing and Transwell assays were performed to investigate the association between gene expression, PI3K/AKT signaling activity, and GC cell invasion and migration. The interaction between uroplakin 1B (UPK1B) and PI3K inhibitor interacting protein 1 (PIK3IP1) was experimentally validated. A set of prognostic signature genes associated with the malignant metastasis of GC was identified, among which UPK1B and chorionic gonadotropin subunit β-5 were demonstrated to be independent predictors of a poor outcome. Notably, UPK1B was validated as an independent biomarker of poor prognosis and a potential therapeutic target in GC. Functional experiments revealed that UPK1B interacted with PIK3IP1 and attenuated the inhibitory effect of PIK3IP1 on the PI3K/AKT signaling pathway, thereby enhancing GC cell invasion and migration. In addition, caudal-related homeobox transcription factor 2 (CDX2) was identified as the transcriptional repressor of UPK1B. The present study delineated prognostic signature genes associated with malignant metastasis of GC. Among them, UPK1B served a pivotal role in regulating GC cell invasion and migration via the CDX2-UPK1B-PIK3IP1-PI3K/AKT axis. These findings provide novel insights into the molecular mechanisms underlying GC metastasis, and highlight UPK1B as a promising biomarker and therapeutic target for future GC therapies.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"184"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13203321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148044906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benefits and mechanisms of polysaccharides derived from traditional Chinese medicine for ulcerative colitis treatment (Review).","authors":"Yuebo Jia, Zheng Jiao, Lingshuo Bai, Gege Li, Lijian Pang","doi":"10.3892/etm.2026.13176","DOIUrl":"10.3892/etm.2026.13176","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by abdominal pain, diarrhea and bloody mucopurulent stools. The UC global incidence is rising and conventional therapies remain limited. Therefore, there is an urgent need for novel treatments. Polysaccharides derived from traditional Chinese medicine (TCM) have emerged as promising candidates due to their multifaceted bioactivities. Preclinical studies have demonstrated that these polysaccharides can regulate immune system pathways, thereby reducing intestinal inflammation and oxidative stress. This protects the intestinal mucosal barrier, enhances tight junction protein expression and modulates the gut microbiota. However, their precise molecular targets and structure-activity associations remain to be fully elucidated. Translational advancement is currently constrained by challenges such as undefined mechanisms, poor oral bioavailability and a lack of clinical validation. Therefore, the present review focused on a number of polysaccharides derived from TCM herbs. The aim of the present review was to systematically analyze their functions and mechanisms for UC prevention and treatment, thus underscoring the necessity for integration of mechanistic discovery with innovative delivery strategies to facilitate the clinical translation of TCM polysaccharides in UC management.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"32 1","pages":"181"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148038668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}