Clinical and Experimental Gastroenterology最新文献

{"title":"Optimization of DMH-Induced Colorectal Carcinogenesis in Rats: A Systematic Meta-Review.","authors":"Alireza Salehi, Fatemeh Yaghoobi, Mostafa Kami, Hamila-Sadat Hashemi Maivan, Hamidreza Habibi, Mohammadreza Mehraban, Sarah Gholami","doi":"10.2147/CEG.S629447","DOIUrl":"10.2147/CEG.S629447","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a major global health concern, and experimental animal models continue to play a key role in understanding its development and in evaluating preventive and therapeutic strategies. Among these, the 1,2-dimethylhydrazine (DMH)-induced rat model is widely used; however, substantial variability in dosing regimens and study design has limited consistency across studies. The present systematic review aimed to synthesize existing evidence on DMH-induced colorectal carcinogenesis in rats, with particular attention to how dose, duration, and route of administration influence pathological outcomes. A comprehensive literature search was conducted across PubMed, Scopus, and Web of Science from January 2010 to December 2025. Eligible studies were screened and analyzed based on predefined inclusion criteria. Data were extracted on induction protocols, histopathological findings, and study characteristics. Across the 430 included studies, notable heterogeneity was observed in experimental protocols. Nevertheless, certain patterns emerged. Higher-dose, shorter-duration regimens were more frequently associated with early preneoplastic lesions such as aberrant crypt foci (ACF), whereas lower-dose, longer-duration protocols tended to be linked with more advanced tumor development. Subcutaneous administration appeared to provide more consistent results compared to other routes. These findings suggest that the choice of protocol should be guided by the intended stage of carcinogenesis under investigation. Importantly, the interpretation of these findings should be approached with caution. Many studies lacked detailed reporting of methodological parameters, and quantitative synthesis was limited by incomplete data. As such, the proposed framework should be viewed as a practical guide rather than a definitive standard. In conclusion, DMH-induced CRC models in rats remain valuable but highly sensitive to experimental design. Greater standardization and more rigorous reporting are needed to improve reproducibility and strengthen the translational relevance of future studies.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"629447"},"PeriodicalIF":2.6,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849941","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":"Advancing Equity and Patient Partnership in Clinical Trials for Inflammatory Bowel Disease: A Model for Inclusive Trial Design.","authors":"David T Rubin, Andres Yarur, Renika Wood, Brian Po-Han Chen, Lisa E Young, Megan Gower, Vijay Yajnik","doi":"10.2147/CEG.S603005","DOIUrl":"10.2147/CEG.S603005","url":null,"abstract":"<p><strong>Purpose: </strong>Efficacy rates of advanced therapies for inflammatory bowel disease (IBD) may be improved by combination therapy approaches, which are being investigated in two ongoing phase 4 clinical trials. To ensure relevancy to wider patient populations, understanding and mitigating barriers to recruitment and enrollment early in study development are crucial. Here, we describe the findings of a unique approach in IBD research to proactively engage patients in study design and in the development of accessible patient-facing materials.</p><p><strong>Methods: </strong>EXPLORER 2.0 (NCT06045754) and ExiGem (NCT06095128) are phase 4, open-label trials evaluating the efficacy and safety of combination therapy with vedolizumab and either adalimumab or ustekinumab in patients with moderate to severe Crohn's disease (CD), and vedolizumab and tofacitinib in patients with moderate to severe ulcerative colitis (UC). During protocol development, 90-minute interviews were conducted with individuals with CD or UC to gain qualitative insights into patient perceptions on the study design and informed consent forms (ICFs). Interview participants were members of Inspire, a global online health community platform, and not aware of the study sponsor.</p><p><strong>Results: </strong>Overall, participants found the concept of achieving remission with combination therapy appealing, although they expressed concerns about its safety. Other concerns included the stringent eligibility criteria and the number of clinic visits and procedures involved in the trials. Participants were generally positive about the inclusion of patient-reported outcomes. Participants suggested the use of clearer language in patient materials, including ICFs, and the inclusion of a visual dosing timeline to clarify treatment schedules. Using the participants' feedback, the study protocols and ICFs have been amended.</p><p><strong>Conclusion: </strong>These interview findings directly informed patient-centric modifications to trial protocols and patient-facing materials for the EXPLORER 2.0 and ExiGem trials with the essential goal of improving patient diversity and recruitment, which have been suboptimal in IBD research.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"603005"},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13508045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825668","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":"Metabolic Dysfunction-Associated Steatotic Liver Disease: Clinical Heterogeneity, Risk Stratification, and Personalized Care.","authors":"Thong Duy Vo","doi":"10.2147/CEG.S618553","DOIUrl":"10.2147/CEG.S618553","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide, reflecting the global epidemic of obesity, type 2 diabetes, and metabolic syndrome. However, MASLD is not a homogeneous condition; rather, it encompasses a broad clinical and biological spectrum ranging from simple steatosis to progressive steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma. This heterogeneity is driven by complex interactions between metabolic dysfunction, genetic susceptibility, environmental exposures, and extrahepatic comorbidities. Recent advances have shifted the paradigm from a \"one-size-fits-all\" approach toward risk stratification and personalized care. Non-invasive tests (NITs), including FIB-4, transient and shear wave elastography, and novel biomarkers, have enabled scalable fibrosis assessment and prognostic stratification in real-world settings. At the same time, emerging therapies targeting metabolic pathways, inflammation, and fibrosis are paving the way for individualized treatment strategies. This review provides an updated and clinically oriented synthesis of MASLD by integrating clinical heterogeneity, phenotype-based disease trajectories, multidimensional risk stratification, and personalized management into a practical framework for precision hepatology. In addition, we summarize recent therapeutic advances, discuss current controversies and implementation challenges, and highlight future directions toward individualized care.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"618553"},"PeriodicalIF":2.6,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13496127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788858","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":"The Metabolic Legacy of Acute Pancreatitis: Post-Pancreatitis Diabetes Mellitus.","authors":"Serge Chooklin, Serhii Chuklin","doi":"10.2147/CEG.S635877","DOIUrl":"https://doi.org/10.2147/CEG.S635877","url":null,"abstract":"<p><p>Post-pancreatitis diabetes mellitus after acute pancreatitis (PPDM-A) is increasingly recognized as a distinct metabolic complication rather than a simple subtype of type 2 diabetes. This narrative review summarizes current evidence on PPDM-A, with emphasis on terminology, diagnostic timing, epidemiology, pathophysiology, risk factors, clinical phenotypes, screening, prevention, and long-term follow-up. A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Google Scholar to identify relevant studies. PPDM-A may develop after mild, moderately severe, or severe acute pancreatitis, although the risk is greatest in patients with pancreatic necrosis, recurrent attacks, exocrine pancreatic dysfunction, obesity, dyslipidemia, fatty liver disease, metabolic comorbidities, and marked in-hospital glycemic variability. A major diagnostic challenge is distinguishing transient stress hyperglycemia and previously unrecognized diabetes from incident PPDM-A. Formal diagnosis should generally be established no earlier than 90 days after the index episode of acute pancreatitis to minimize misclassification due to transient stress-related dysglycemia. Follow-up assessment should combine fasting plasma glucose and HbA1c, whereas a 75-g oral glucose tolerance test (OGTT) may provide greater sensitivity during early recovery, particularly when HbA1c is unreliable, results are borderline or discordant, or isolated postprandial dysglycemia is suspected. Current evidence indicates that PPDM-A develops through interacting pathogenic domains, including pancreatic endocrine injury with impaired β-cell reserve, metabolic dysregulation characterized by insulin resistance and persistent inflammation, exocrine pancreatic dysfunction with nutritional consequences, and emerging mechanisms involving gut microbiome alterations, bile acid-FGF19 signaling, and extracellular vesicle-mediated communication. Available data support a trajectory-based model in which some patients recover normal glucose metabolism, some develop persistent intermediate dysglycemia, and others progress to overt diabetes over months or years. Structured post-discharge surveillance, risk-stratified follow-up, assessment of exocrine dysfunction, and prevention of recurrent pancreatic injury are essential for improving early detection, reducing diagnostic misclassification, and optimizing long-term clinical outcomes.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"635877"},"PeriodicalIF":2.6,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13478238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788875","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":"Splenic Steatopathy: A Clinical and Experimental Framework for Lipid-Associated Splenic Pathology.","authors":"Vishal G Shelat","doi":"10.2147/CEG.S628370","DOIUrl":"https://doi.org/10.2147/CEG.S628370","url":null,"abstract":"<p><p>The spleen is usually viewed as a hematologic, vascular and immune organ, but rarely within lipid-associated disease. This review proposes splenic steatopathy as a provisional clinical and experimental framework rather than an established diagnosis or a splenic equivalent of fatty liver disease. Evidence is organized into pre-splenic drivers, intra-splenic pathology and post-splenic consequences. Upstream drivers include metabolic dysfunction-associated steatotic liver disease, obesity, severe hypertriglyceridemia, lysosomal storage disorders, drug-induced phospholipidosis, altered lymphatic lipid handling and portal-hemodynamic stress. Spleen-level findings include altered volume, attenuation, stiffness or metabolic activity; lipid-laden histiocytes; lysosomal or phospholipid storage; and immune-cell remodeling. Potential downstream relevance includes cytopenias, immune dysfunction, infection vulnerability, diagnostic redirection, cancer-associated immune biology and perioperative risk. Human evidence currently consists mainly of observational imaging studies and rare tissue reports; animal studies provide mechanistic support, while several proposed clinical links remain hypotheses. No validated diagnostic criteria, imaging thresholds or biomarkers currently exist. The framework may help distinguish unexplained splenomegaly from common mimics and, if validated, support long-term risk stratification for infection and malignancy in patients with metabolic liver disease. Future studies should prioritize spleen-specific imaging methods, tissue-imaging correlation, lipidomics, immune phenotyping and prospective outcome validation.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"628370"},"PeriodicalIF":2.6,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13476756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758104","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":"Gut Microbiome and Short-Chain Fatty Acid Alterations After Cardiopulmonary Bypass are Associated with Nutritional and Functional Impairment in Young Children with Congenital Heart Defects.","authors":"Shoira Abdusalamovna Agzamova, Faniya Rashidovna Babadjanova","doi":"10.2147/CEG.S600414","DOIUrl":"10.2147/CEG.S600414","url":null,"abstract":"<p><strong>Background: </strong>Cardiac surgery with cardiopulmonary bypass (CPB) in young children is associated with systemic stress, gastrointestinal dysfunction, and impaired nutritional recovery. The role of gut microbiome disruption and short-chain fatty acid (SCFA) metabolism in these processes remains insufficiently studied.</p><p><strong>Objective: </strong>To evaluate changes in gut microbiome composition, SCFA profiles, and nutritional status in children aged 0-3 years after CPB, and to assess their association with postoperative feeding intolerance and impaired growth.</p><p><strong>Methods: </strong>This prospective observational study included 20 children undergoing cardiac surgery with CPB. Stool samples were collected preoperatively and during the early postoperative period. Microbiota composition was assessed using culture-based microbiological methods, and fecal SCFA concentrations were measured by gas chromatography. Clinical, anthropometric, and laboratory parameters were assessed, and their associations with CPB characteristics and microbiome alterations were analyzed.</p><p><strong>Results: </strong>The postoperative period was characterized by significant intestinal dysbiosis, including reduced abundance of beneficial bacteria (Bifidobacterium, Lactobacillus, Bacteroides) and decreased SCFA-producing taxa. Fecal butyrate and propionate levels were significantly reduced. These changes were associated with increased intestinal inflammation, feeding intolerance, impaired nutrient absorption, and insufficient weight gain. The severity of dysbiosis correlated with CPB duration.</p><p><strong>Conclusion: </strong>CPB in early childhood is associated with disruption of gut microbiota and reduced SCFA production, which are linked to postoperative feeding intolerance and impaired nutritional recovery. Targeted monitoring and modulation of the gut microbiome may improve clinical outcomes in pediatric cardiac surgery patients.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"600414"},"PeriodicalIF":2.6,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249314","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":"Irritable Bowel Syndrome Prevalence in Patients with Inflammatory Bowel Disease in Remission: Single-Center Experience.","authors":"Olga Golubovic, Tamara Knezevic Ivanovski, Djordje Kralj, Milos Mitrovic, Aleksandar Milić, Petar Svorcan, Srdjan Markovic","doi":"10.2147/CEG.S582517","DOIUrl":"10.2147/CEG.S582517","url":null,"abstract":"<p><strong>Background: </strong>Irritable bowel syndrome (IBS) and inflammatory bowel diseases (IBD) are characterized by features of abdominal pain and changes in bowel habits, making it hard to differentiate between the two. Early studies that estimated prevalence of IBS in IBD patients defined remission based only on clinical scores, potentially overestimating IBS symptoms and underestimating subclinical inflammation. The aim of this study was to determine prevalence of IBS in IBD patients who are treated with biologics and have reached clinical, biologic and endoscopic remission, thereby applying a more stringent definition of remission.</p><p><strong>Methods: </strong>This single-center cross-sectional study included 136 patients (68 patients with Crohn's disease and 68 with ulcerative colitis) who are treated with biologics from December 2022 to June 2023 and have reached clinical, biologic and endoscopic remission. Clinical remission was defined as Crohn's disease activity index (CDAI) ≤ 150 for patients with Crohn's disease (CD), and Mayo partial score ≤ 1 for patients with ulcerative colitis (UC). Biologic remission was defined as faecal calprotectin (FCP) ≤ 250 ug/g, and endoscopic remission was defined as the absence of ulcerations for CD and Mayo subscore ≤ 1 for UC patients. The presence of IBS was defined by Rome IV criteria.</p><p><strong>Results: </strong>A total of 28 (20.6%) patients in complete remission reported symptoms consistent with IBS, based on Rome IV criteria. The prevalence of IBS was higher in patients with Crohn's disease than in those with ulcerative colitis (CD 27.9% (19/68) vs UC 13.2% (9/68), <i>p</i> = 0.034). Females and smokers with Crohn's disease are more likely to report IBS symptoms.</p><p><strong>Conclusion: </strong>Prevalence of IBS symptoms in IBD patients varies according to how remission is defined. When using stringent clinical, biological and endoscopic remission criteria, 20% of patients present with IBS symptoms, more commonly in those with CD.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"582517"},"PeriodicalIF":2.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13242762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204412","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":"Erratum: Review of the Patient Burden and Therapeutic Landscape of Irritable Bowel Syndrome with Constipation in the United States [Corrigendum].","authors":"","doi":"10.2147/CEG.S618800","DOIUrl":"https://doi.org/10.2147/CEG.S618800","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.2147/CEG.S464375.].</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"618800"},"PeriodicalIF":2.3,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13242204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197498","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":"Primary Colorectal Signet Ring Cell Carcinoma and the Risk of Multiple Primary Gastrointestinal Malignancies: A Retrospective Cohort Based on SEER Database from 2000-2021.","authors":"Belal Mohamed Hamed, Asmaa Ellaithy, Alzahraa Faris Alesawy, Alhareth Alhusban, Nahla Ali, Bushra Al-Shaikh, Eslam Mohamed Elshennawy, Sally Ali Elbadry","doi":"10.2147/CEG.S588726","DOIUrl":"10.2147/CEG.S588726","url":null,"abstract":"<p><strong>Background: </strong>Signet-ring cell carcinoma (SRCC) is a rare subtype of colorectal cancer, constituting 0.5-2.5% of all adenocarcinomas. It is characterized by signet ring cells as the dominant malignant cell type. Developing gastrointestinal (GI) second primary malignancies (SPMs) after SRCC is a rare event reported in the literature and insufficiently addressed. This study aimed to explore this gap and provide updated evidence about this rare cancer.</p><p><strong>Methods: </strong>Data were extracted from the Surveillance, Epidemiology, and End Results (SEER) database. Standardized incidence ratio (SIR) analyses with multiple outcome assessment were performed, applying a two-month latency exclusion period to evaluate the risk of GI SPMs in patients diagnosed with primary colorectal SRCC. The SIR was calculated as observed/expected (O/E), with excess absolute risk (EAR) per 10,000. Significance was achieved at 0.05 with a 95% confidence interval (CI).</p><p><strong>Results: </strong>There was an increased risk for GI SPMs after SRCC in the 2-11 months interval (O/E=2.49, P<0.05, EAR=37.31), and over 10 years of follow-up (O/E=3.08, P<0.05, EAR=59.20). Small intestine SPMs in the 2-11 months interval had an O/E of 4.17 (P<0.05, 95% CI: 0.11-23.26, EAR=1.97), with an overall O/E of 9.62 (P<0.05, EAR=6.32). No events of GI SPMs were observed among young patients during follow-up (O/E=1.05, P>0.05, EAR=0.12). Young patients had lack of observed events for GI SPMs (O/E=0.00, EAR=-0.15), compared to middle-aged (O/E=7.66, P<0.05) and elderly patients (O/E=2.36, P<0.05). Patients received chemotherapy showed a slightly higher observed incidence of SPMs (O/E=2.39, P<0.05, EAR=49.29); however, this finding should be interpreted cautiously given known limitations of chemotherapy data within the SEER database.</p><p><strong>Conclusion: </strong>Patients diagnosed with colorectal SRCC are at a significantly increased risk of developing GI SPMs. Given the poor overall prognosis of colorectal SRCC, early surveillance protocols must be carefully contextualized at short intervals (6-12 months) for early detection of GI SPMs. However, a reduced intensity surveillance is recommended beyond 3-5 years to integrate prevention with long-term follow-up. Recommendations should be tailored according to patients' risk profiles with individualized patient focused programs.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"588726"},"PeriodicalIF":2.6,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13222554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142779","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":"Assessment of the Biological Effect of Oral Ginkgolic Acid Liposome Nanoparticles for Treating Refractory <i>Helicobacter pylori</i> Infection.","authors":"Jingwen Xu, Chengbo Zhang, Yan Jiang, Rumeng Wang, Yang Liu, Ning Zhang, Yugang Liu, Lizhou Jia","doi":"10.2147/CEG.S590424","DOIUrl":"10.2147/CEG.S590424","url":null,"abstract":"<p><strong>Objective: </strong>To explore the antibacterial effect of ginkgolic acid (GA) modified into liposome nanoparticles (TLM@GA) against <i>Helicobacter pylori</i> and investigate the antibacterial mechanism involved to provide a lead drug for radical clinical treatment.</p><p><strong>Methods: </strong>A new complex that improved GA stability and bioavailability was constructed using liposome nanoparticles (TLM@GA). The construction of the complex was verified by Fourier transform infrared spectroscopy, scanning electron microscopy, Zeta potential, and particle size detection, and its physicochemical properties were comprehensively evaluated. An acute gastritis model was also established using C57BL/6 mice, in which the in vivo therapeutic effect of TLM@GA was evaluated by detecting the colonization amount of the clinical multi-resistant strain HPBS001 in the gastric mucosa. Additionally, the pathological inflammation of the gastric mucosa was observed with H&E staining, apoptosis of gastric mucosal cells was observed with TUNEL staining, and the expression of serum inflammatory factors was detected with enzyme-linked immunosorbent assay. The in vivo safety of TLM@GA was evaluated by detecting its effect on mouse body weight and the damage to the stomach, liver, spleen, and kidneys.</p><p><strong>Results: </strong>The TLM@GA complex had excellent stability and dispersibility. The minimum inhibitory concentration of GA against <i>H. pylori</i> strains was 16-32 μg/mL, and that of TLM@GA was 0.25-0.5 μg/mL. After GA was modified into TLM@GA, its antibacterial activity was 32-128 times higher. After treatment with TLM@GA (28 mg/kg), the colonization of <i>H. pylori</i> in the gastric mucosa was significantly reduced, which was better than that in the omeprazole and amoxicillin (dual-therapy) and GA groups. Apoptotic and inflammatory cells in the gastric mucosa were significantly reduced, indicating alleviated inflammation. After treatment, the expression levels of major inflammatory factors were significantly decreased. There was no significant change in body weight when mice were intragastrically administered 140 mg/kg TLM@GA for 1 week, and no obvious pathological damage was found in the stomach, liver, spleen, or kidneys.</p><p><strong>Conclusion: </strong>TLM@GA had excellent stability, efficient release, and good loading capacity efficiency. It was significantly superior to GA in terms of in vitro antibacterial activity, had low toxicity, was not prone to drug resistance, and demonstrated high safety. TLM@GA demonstrated a good antibacterial effect in the in vivo acidic environment, effectively slowing the apoptosis of gastric mucosal cells and significantly reducing levels of inflammatory factors, alleviating the inflammatory response.</p>","PeriodicalId":10208,"journal":{"name":"Clinical and Experimental Gastroenterology","volume":"19 ","pages":"590424"},"PeriodicalIF":2.6,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13180319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971060","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}