BMC Gastroenterology最新文献

{"title":"Collagen turnover biomarkers to predict outcome of patients with biliary cancer.","authors":"Leonard Kaps, Muhammed A Genc, Markus Moehler, Stephan Grabbe, Jörn M Schattenberg, Detlef Schuppan, Rasmus Sund Pedersen, Morten A Karsdal, Philipp Mildenberger, Annett Maderer, Nicholas Willumsen","doi":"10.1186/s12876-025-03645-0","DOIUrl":"10.1186/s12876-025-03645-0","url":null,"abstract":"<p><strong>Background: </strong>The collagen-rich tumor stroma plays a crucial role in biliary tract cancer (BTC). Collagen biomarkers of type I collagen (reC1M), type III collagen (PRO-C3), type IV collagen (C4G), type VIII collagen (PRO-C8), type XI collagen (PRO-C11), type XVII collagen (PRO-C17) and type VIII collagen (TUM) may be used as potential non-invasive biomarkers.</p><p><strong>Methods: </strong>We measured the seven biomarkers of collagen turnover in sera of 72 patients with BTC at baseline and after first and second chemotherapy cycle (CTX). Markers were also assessed in sera of 50 healthy controls and compared to levels of patients at baseline. The diagnostic and prognostic value of the markers was evaluated for overall survival (OS) and progression-free survival (PFS).</p><p><strong>Results: </strong>Patients had a median age of 65 years (IQR 57-70), while healthy controls were younger, with a median age of 46 years (IQR 38-54). The majority of patients (62%) were diagnosed with intrahepatic bile duct adenocarcinoma. Except C4G, all collagen turnover markers were significantly (p < 0.001) increased in serum from patients with BTC compared to healthy controls. PRO-C3 was the best marker to discriminate between patients with BTC and controls, reaching an area under a receiver operating characteristic (AUROC) of 0.98 (95% CI 0.95; 0.99) with a sensitivity (92%) and specificity (94%) balanced cutoff of 77.3 ng/ml. Patients with high levels (cohort separated by median split) of PRO-C8 (HR 2.85, 95% CI 1.42; 5.73) followed by C3M (HR 2.33, 95% CI 1.2; 4.5), PRO-C3 (HR 3.09, 95% CI 1.5; 6.36) and CA 19-9 (HR 2.52, 95% CI 1.37; 4.64) as reference biomarker had a shorter OS. Notably, only the novel marker PRO-C8 was also predictive of PFS (HR 3.26, 95% CI 1.53; 6.95). Associations with survival outcomes remained significant after adjusting for relevant risk factors (CA 19-9 and CEA at baseline, age, presence of metastases, weight, height and gender).</p><p><strong>Conclusion: </strong>The collagen turnover markers PRO-C8, C3M, PRO-C3 and the established biomarker CA 19-9 were prognostic for OS in patients with BTC while only PRO-C8 was also predictive for PFS. PRO-C3 showed the best diagnostic performance to discriminate between patients with BTC and controls.</p><p><strong>Trial registration: </strong>Trial registration number and date of registration NCT00661830 (NCT number) 15 April 2008 Trial registry The complete registry can found under: https://clinicaltrials.gov/study/NCT00661830?tab=table#administrative-information (last accessed 01/2025) Principal investigator and study sponsor Markus Moehler, MD Johannes Gutenberg University Mainz.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"53"},"PeriodicalIF":2.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic investigation and the optimal dose based on baicalin in the treatment of ulcerative colitis-A preclinical systematic review and meta-analysis.","authors":"Jinchen Chong, Zepeng Chen, Jiaze Ma, Linhai He, Yijia Zhu, Zhihua Lu, Zhengxi Qiu, Chen Chen, Yugen Chen, Feng Jiang","doi":"10.1186/s12876-025-03629-0","DOIUrl":"10.1186/s12876-025-03629-0","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) is a type of inflammatory bowel disease, and current treatments often fall short, necessitating new therapeutic options. Baicalin shows therapeutic promise in UC animal models, but a systematic review is needed.</p><p><strong>Methods: </strong>A systematic search was conducted across databases including PubMed, EBSCO, Web of Science, and Science Direct, up to March 2024, identifying randomized controlled trials (RCTs) examining baicalin's impact on UC in animal models. Seventeen studies were selected through manual screening. Meta-analyses and subgroup analyses utilized Rev Man 5.3 and Stata 15.0 software to assess symptom improvement.</p><p><strong>Results: </strong>From 1304 citations, 17 were analyzed. Baicalin significantly modulated various biomarkers: HCS (SMD = -3.91), DAI (MD = -2.75), spleen index (MD = -12.76), MDA (SMD = -3.88), IL-6 (SMD = -10.59), IL-1β (SMD = -3.98), TNF-α (SMD = -8.05), NF-κB (SMD = -5.46), TLR4 (MD = -0.38), RORγ (MD = -0.89), MCP-1 (MD = -153.25), MPO (SMD = -7.34), Caspase-9 (MD = -0.93), Caspase-3 (MD = -0.45), FasL (MD = -1.20)) and enhanced BWC (MD = 0.06), CL (MD = 1.39), ZO-1 (MD = 0.44), SOD (SMD = 3.04), IL-10 mRNA (MD = 3.14), and FOXP3 (MD = 0.45) levels. Baicalin's actions may involve the PI3K/AKT, TLR4/NF-κB, IKK/IKB, Bcl-2/Bax, Th17/Treg, and TLRs/MyD88 pathways. Optimal therapeutic outcomes were predicted at dosages of 60-150 mg/kg over 10-14 weeks.</p><p><strong>Conclusion: </strong>Baicalin demonstrates a multifaceted therapeutic potential in UC, attributed to its anti-inflammatory, antioxidant, anti-apoptotic, and intestinal barrier repair properties. While higher doses and longer treatments appear beneficial, further research, particularly human clinical trials, is necessary to verify its effectiveness and safety in people.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"50"},"PeriodicalIF":2.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liver cancer risk and changes in lifestyle habits after successful hepatitis C virus therapy post-DAA HCV therapy: lifestyle changes and liver cancer risk.","authors":"Núria Granel, Gemma Iserte, Concepció Bartres, Neus Llarch, Anna Pla, Víctor Sapena, Zoe Mariño, Sabela Lens, Ramón Vilana, Isabel Nuñez, Anna Darnell, Ernest Belmonte, Ángeles García-Criado, Alba Díaz, Marco Sanduzzi-Zamparelli, Carla Fuster, Sergio Muñoz-Martínez, Carmen Ayuso, Jordi Rimola, Alejandro Forner, Alexandre Soler, Ferran Torres, José Ríos, Jordi Bruix, Andrew M Moon, Xavier Forns, María Reig","doi":"10.1186/s12876-025-03611-w","DOIUrl":"10.1186/s12876-025-03611-w","url":null,"abstract":"<p><strong>Background: </strong>The eradication of the Hepatitis C Virus (HCV) reduce the risk of liver cancer (LC), but lifestyle changes after cure may counterbalance its benefit. Our study investigates lifestyle changes that occur in HCV patients with Sustained Virological Response (SVR) after direct-acting antiviral (DAA) treatment.</p><p><strong>Methods: </strong>In this prospective, single-center study, HCV patients with advanced liver disease (F3/F4) treated and cured with DAA were invited to fill a lifestyle habits questionnaire in and perform abdominal ultrasound (US), blood extraction and anthropometric measurements within the 1st month after SVR and every 6 months thereafter until 48 months of follow-up, LC development, death, or loss to follow-up.</p><p><strong>Results: </strong>This prospective cohort included 182 patients with SVR after DAA in this first analysis through the 4 years of follow-up. At the time of SVR, 65.9% had cirrhosis, median BMI was 27.1 kg/m², 74.2% were overweight or obese and 6.6% had an US with hepatic steatosis. Within a year of SVR, 9% of males and 4% of females progressed from normal weight to overweight/obesity and 19.4% increased alcohol consumption. At 48 months, there were statistically significant increases in BMI (0.75, p = 0.001) and alcohol consumption (6.4% p = 0.007).</p><p><strong>Conclusions: </strong>In this prospective cohort, successful HCV therapy was followed by significant changes in lifestyle habits translating into increases in BMI and alcohol consumption. These post-SVR changes raise concerns that the chemopreventive benefits of HCV cure may be counterbalanced by increased risks of liver disease progression and LC development from metabolic risk factors and alcohol use. Post-SVR, patients may benefit from intensive counseling and pharmacotherapy to address obesity and alcohol use.</p><p><strong>Trial registration/ clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"51"},"PeriodicalIF":2.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary phytochemical index and the risk of gallstone disease: a case-control study.","authors":"Mohammad Abdulmohsin Jebur, Ghufran Lutfi Ismaeel, Haitham Mukhklif Salim, Ammar Hussein Ahmed, Israa Habeeb Naser","doi":"10.1186/s12876-025-03622-7","DOIUrl":"10.1186/s12876-025-03622-7","url":null,"abstract":"<p><p>BACKGROUNDSː: Dietary phytochemical index (DPI) is an inexpensive method for estimating the amounts of phytochemicals in foods. No study has investigated the association between DPI and gallstones disease (GSD). Therefore, we conducted a case-control study in adults to assess the relationship between DPI and the risk of gallstones.</p><p><strong>Methods: </strong>The study was conducted at the general surgical consultation departments of two major multispecialty hospitals in Baghdad: Al-Yarmook and Al Karama Teaching Hospitals. It involved 250 patients with gallstones and 250 controls. DPI was calculated based on data collected from a 168-item validated food frequency questionnaire. Sociodemographic data, physical activity, and anthropometric measures were determined.</p><p><strong>Results: </strong>In the initial analysis, the highest tertile of total PI compared to the lowest tertile was found to be associated with a lower risk of galleston (OR and 95% CI = 0.61 (0.41-0.93), p for trend = 0.027). This significant association remained even after adjusting for age and sex, and the odds ratio slightly strengthened. In the final adjusted model, which accounted for additional confounders such as physical activity, BMI, smoking, socioeconomic status (SES), and dietary intake of energy, participants in the highest tertile of total PI still had a lower risk of gallston compared to those in the lowest tertile (OR and 95% CI = 0.51 (0.28-0.90), p for trend = 0.031.</p><p><strong>Conclusion: </strong>We found evidence of a negative relationship between the dietary phytochemical index and the risk of gallstones, even after accounting for potential confounding variables. As a result, it may be advisable to include more phytochemical-rich foods in dietary approaches aimed at preventing gallstones. However, additional studies are needed to confirm the link between the dietary phytochemical index and gallstone.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"52"},"PeriodicalIF":2.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative proteomic studies of the intestinal mucosa provide new insights into the molecular mechanism of ulcerative colitis.","authors":"Yandong Guo, Dahal Pabitra, Lei Pan, Lanbo Gong, Aimin Li, Side Liu, Jing Xiong","doi":"10.1186/s12876-025-03647-y","DOIUrl":"10.1186/s12876-025-03647-y","url":null,"abstract":"<p><strong>Background: </strong>Differentiation between ulcerative colitis (UC) and other intestinal inflammatory diseases is difficult, and the precise etiology of UC is poorly understood. Thus, there is a need for novel diagnostic and prognostic biomarkers for UC.</p><p><strong>Methods: </strong>Intestinal mucosal biopsy tissue specimens of inflamed (ulcerative colitis-inflamed, UC-I) and non-inflamed (ulcerative colitis-noninflamed, UC-N) tissue were obtained simultaneously during colonoscopy from newly diagnosed UC patients prior to any treatments. Label-free liquid chromatography tandem mass spectrometry (LC-MS/MS) quantitative proteomics was used to detect proteomic differences between UC-I, UC-N, and normal control subjects (n = 5). Proteins with a fold-change > 1.5 and P < 0.05 between groups were considered to be differentially expressed (DEPs). Candidate biomarkers were further verified in 8 patients of each group by parallel reaction monitoring (PRM) (a prospective cohort, n = 8). Expression of TXNDC5 was quantified using immunohistochemistry (IHC).</p><p><strong>Results: </strong>A total of 4,788 proteins were identified. Multiple upregulated pathways, including leukocyte trans-endothelial migration and natural killer (NK) cell-mediated cytotoxicity, were identified. Network analysis showed that proteins were involved in 4 pathways in UC-I and 3 pathways in UC-N tissues, and participated in protein-protein interactions. Increased expression of 9 DEPs, including TXNDC5, EPX, and ITGAM were detected in UC patients compared to normal control subjects. Subsequent verification of the 9 DEPs by PRM confirmed the reliability of the mass spectrometry data. TXNDC5 expression was significantly increased in UC.</p><p><strong>Conclusions: </strong>The pathways, networks, and proteins identified in this study may provide new insights into the molecular pathogenesis of UC. Further studies are required to determine if the proteins identified may help in the diagnosis and treatment of UC.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"48"},"PeriodicalIF":2.5,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Which scoring systems are useful for predicting the prognosis of lower gastrointestinal bleeding? Old and new.","authors":"Ku Bean Jeong, Hee Seok Moon, Kyung Ryun In, Sun Hyung Kang, Jae Kyu Sung, Hyun Yong Jeong","doi":"10.1186/s12876-025-03638-z","DOIUrl":"10.1186/s12876-025-03638-z","url":null,"abstract":"<p><strong>Background: </strong>The incidence of lower gastrointestinal bleeding is on the rise, prompting the creation of various scoring systems to forecast patient's outcomes. But there is no single unified scoring system and these scoring systems clinical data are small and not worldwide.</p><p><strong>Aims: </strong>To evaluate how different scoring systems predict mortality and prolonged hospital stay (≥ 10 days).</p><p><strong>Methods: </strong>A retrospective review was conducted on the medical records of 4417 patients who presented with hematochezia at the emergency department from January 2016 to December 2022. We evaluated the predictive accuracy of various scoring systems for 30-day mortality and prolonged hospital stay (≥ 10 days) by analyzing the areas under the receiver-operating characteristic curves, taking into account factors such as patient age, laboratory findings, and comorbidities (ABC); AIMS 65; Glasgow-Blatchford; Oakland; Rockall(pre-endoscopy); SHA₂PE; and CHAMPS scores.</p><p><strong>Results: </strong>We analyzed data from 1000 patients (mean age 66 years, 56.1% men, mean hospital stay 9.4 days) with lower gastrointestinal bleeding confirmed by any other means including DRE, colonoscopy and CT. The 30-day mortality rate was 3.7%. The primary etiologies of lower gastrointestinal bleeding were identified as ischemic colitis and diverticular bleeding, accounting for 18.8% and 18.5% of cases, respectively. In terms of forecasting 30-day mortality, the AIMS 65, CHAMPS, and ABC scoring systems demonstrated superior performance (p < 0.001). For predicting prolonged hospital stay, the SHA2PE score exhibited the highest accuracy among all evaluated systems (p < 0.001).</p><p><strong>Conclusions: </strong>The newly developed scoring systems demonstrated superior accuracy in forecasting outcomes for patients with lower gastrointestinal bleeding, and the results of this study demonstrate that these scoring systems can be applied in clinical practice.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"49"},"PeriodicalIF":2.5,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuregulin1 ameliorates metabolic dysfunction-associated fatty liver disease via the ERK/SIRT1 signaling pathways.","authors":"Chengan Xu, Shouhao Wang, Di Meng, Mingshan Wang, Rong Yan, Yining Dai","doi":"10.1186/s12876-025-03632-5","DOIUrl":"10.1186/s12876-025-03632-5","url":null,"abstract":"<p><strong>Background: </strong>Neuregulin (NRG) family is involved in energy metabolism, among which NRG1 is a neuregulin proved to play a protective role in MAFLD cells. But the presice echanism has not been fully illustrated. This study aimed to investigate the role of NRG1 via the ERK/SIRT1 signaling in the pathogenesis of MAFLD.</p><p><strong>Methods: </strong>C57BL/6 mice were fed with high-fat diet for 8 weeks, and then injected with NRG1 (0.3 mg/kg/d) and PD98059 (0.3 mg/kg/d) via tail vein for 5 weeks. HepG2 cells induced by oleic acid and palmitic acid were treated with 20ng/mL NRG1 and 10µmol/L PD98059. The changes of histopathological, biochemical indexes, inflammatory factors, lipid metabolism, apoptosis and autophagy parameters were measured.</p><p><strong>Results: </strong>The expressions of NRG1 in MAFLD cell and animal models were significantly lower than that in the control group. After the intervention of ERK inhibitor PD98059, the expression of NRG1 decreased significantly in vivo, but no significant change was observed in vitro. Moreover, NRG1 ameliorated hepatic steatosis, enhanced cell viability, reduced cell apoptosis, and attenuated liver injury both in vitro and in vivo. After NRG1 intervention, the expressions of ERBB2, ERBB3, p-ERK1/2, SIRT1 and p-FOXO1 as well as the LC3II/I ratio in MAFLD cells and liver tissues of MAFLD mice were significantly increased, while the expression of SREBP1c was decreased. The aforementioned therapeutic effect of NRG1 was lost after the intervention of PD98059.</p><p><strong>Conclusion: </strong>NRG1 might play a protective role in the pathogenesis of MAFLD by activating the downstream ERK1/2 through ErbB2-ErbB3, which promotes the expression of SIRT1 and autophagy markers. This study might indicate a new therapeutic strategy for MAFLD.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"47"},"PeriodicalIF":2.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amarogentin suppresses cell proliferation and EMT process through inducing ferroptosis in colorectal cancer.","authors":"Chao Wang, Zihao You, Guoqing Zhou, Juanjuan Dong, Sihao Tong, Guoping Sun","doi":"10.1186/s12876-025-03649-w","DOIUrl":"10.1186/s12876-025-03649-w","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is one common tumor with the high death rate, and badly affects the normal lives of CRC patients. Amarogentin (AG) has been found to exhibit regulatory roles and join into the progression of multiple diseases. However, the regulatory impacts and associated molecular mechanisms of AG in CRC progression keep unclear.</p><p><strong>Methods and results: </strong>In this study, it was demonstrated that AG weakened CRC cell viability in a concentration- and time-dependent manner. In addition, AG accelerated cell apoptosis by triggering ferroptosis. The cell invasion and EMT process were restrained after AG treatment, but these impacts were reversed after Fer-1 addition. Moreover, it was uncovered that AG retarded Nrf2/HO-1/GPX4 activation. Additionally, AG modulated PTC cell viability and stimulated ferroptosis. At last, it was illustrated that AG suppressed tumor growth in vivo.</p><p><strong>Conclusion: </strong>In conclusion, it was disclosed that AG suppressed cell proliferation and EMT process through inducing ferroptosis in CRC, and retarded Nrf2/HO-1/GPX4 activation. This discovery suggested that AG may be one effective drug for ameliorating CRC progression.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"46"},"PeriodicalIF":2.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell damage by inhibiting autophagy.","authors":"Na Liu, Pu Zhao, Ping Cao, JunPeng Hui, YongKang Pan, Jiwen Cheng","doi":"10.1186/s12876-025-03640-5","DOIUrl":"10.1186/s12876-025-03640-5","url":null,"abstract":"<p><strong>Background: </strong>The increased apoptosis of bile duct epithelial cells (BECs) due to some damage factors is considered the initiating factor in the occurrence and progression of biliary atresia (BA). Vitamin D receptor (VDR) is thought to play a crucial role in maintaining the intrinsic immune balance and integrity of bile duct epithelial cells (BECs). To investigate the role of VDRs in the pathogenesis and progression of BA using in vitro and in vivo models.</p><p><strong>Materials and methods: </strong>The VDR expression levels in intrahepatic bile duct epithelial cells (IBDECs) in pediatric patients with BA were examined using immunohistochemical analysis. The correlation of the VDR levels with the incidence of refractory cholangitis after Kasai portoenterostomy (KPE) and the autologous liver survival time was analyzed. The levels of genes and proteins involved in related pathways were examined using quantitative real-time polymerase chain reaction and western blotting, respectively. The secretory levels of inflammatory factors were analyzed using enzyme-linked immunosorbent assay. A BA mouse model was established through the intraperitoneal sequential injection of rhesus rotavirus (RRV). The role of VDR in the pathogenesis and progression of BA was examined using in vitro and in vivo models. Retrospective analysis of patients with BA to examine the therapeutic efficacy of VDR activators on BA.</p><p><strong>Results: </strong>15 pediatric BA patients exhibiting VDR downregulation in IBDECs showed a higher incidence of refractory cholangitis after Kasai portoenterostomy (p = 0.037) and a lower native liver survival time compare to 23 BA patients without VDR downregulation (p = 0.032). 1,25-VD3 inhibited the degree of autophagy induction in HIBECs by poly(I: C) (p < 0.05), mitigated poly(I: C)-induced BEC damage and apoptosis by inhibiting autophagy (p < 0.05). 1,25-VD3 significantly suppressed the poly(I: C)-induced downregulation of SRC (p < 0.05) and ERK1/2 phosphorylation (p < 0.05). 1,25-VD3 exert a protective effect against RRV-induced BEC damage by inhibiting autophagy in BA mouse model. The incidence of cholangitis and the native liver survival time after surgery in the calcitriol-treated group was significantly lower than that in the control group. (p = 0.033, p = 0.035, respectively).</p><p><strong>Conclusions: </strong>VDR activator mitigated dsRNA-induced BEC damage and apoptosis by inhibiting autophagy in vitro and in vivo. The 1,25-VD3/VDR/Src axis alleviated poly(I: C)-induced HIBEC damage and apoptosis through the PLA2/PKC/ERK pathway.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"44"},"PeriodicalIF":2.5,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between systemic inflammatory biomarkers and metabolic dysfunction associated steatotic liver disease: a cross-sectional study of NHANES 2017-2020.","authors":"Xin Qiu, Shuang Shen, Nizhen Jiang, Yifei Feng, Guodong Yang, Donghong Lu","doi":"10.1186/s12876-025-03625-4","DOIUrl":"10.1186/s12876-025-03625-4","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a primary cause of chronic liver disease, with potential progression to cirrhosis and hepatocellular carcinoma (HCC). Although systemic inflammatory biomarkers are associated with liver diseases, their specific role in MASLD remains unclear. This study examines the association between systemic inflammatory biomarkers and MASLD.</p><p><strong>Methods: </strong>This cross-sectional study enrolled 6613 adults aged 20 years or older from the National Health and Nutrition Examination Survey (NHANES) spanning from 2017 to March 2020. Among these participants,, 34.67% were aged 40-59 years, 50.85% were female, and 63.26% were Non-Hispanic White. We investigated 10 inflammatory biomarkers: ALI, SIRI, SII, SIPS, IBI, NLR, PLR, CAR, LMR, and PNI. Logistic regression models were performed to assess the linear association between systemic inflammatory biomarkers and MASLD. Restricted cubic spline (RCS) regression was employed to explore potential nonlinear relationships between biomarkers and MASLD risk. Additionally, subgroup analyses were conducted to examine the influence of various demographic and clinical characteristics on the observed associations.</p><p><strong>Results: </strong>After adjusting for key confounders, NLR and PLR exhibited negative association with MASLD risk, while ALI, CAR, and PNI exhibited the opposite association (P < 0.05). Most biomarkers, including ALI, SIRI, IBI, CAR, LMR, and PNI, exhibited significant non-linear correlations with MASLD (P < 0.05). Subgroup analyses revealed substantial age-related differences in the association between ALI and MASLD risk, as well as varying relationships between PNI and MASLD risk across various cardiovascular outcomes (P < 0.05).</p><p><strong>Conclusion: </strong>Systemic inflammatory biomarkers are significantly associated with MASLD risk. Large-scale prospective studies are warranted to confirm these findings and elucidate the underlying mechanisms.</p>","PeriodicalId":9129,"journal":{"name":"BMC Gastroenterology","volume":"25 1","pages":"42"},"PeriodicalIF":2.5,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}