Duodenal web is rare in children, and reports of symptomatic cases with delayed presentation are even scarcer. This paper reports a 19-month-old female toddler admitted to hospital due to recurrent vomiting. Imaging examinations suggested duodenal obstruction, with an initial consideration of superior mesenteric artery syndrome or space-occupying lesion of the duodenum. In this case, circumferential thickening of the muscular layer of the duodenal wall was detected by endoscopic ultrasound (EUS), and pathological biopsy was performed simultaneously. Neoplastic lesions were systematically excluded, and the diagnosis of delayed-presentation duodenal web was established. The toddler successfully underwent endoscopic web incision eventually, avoiding open surgery. Postoperatively, the vomiting symptom was completely relieved without any complications. EUS clearly delineates the layered structure of the duodenal wall, thereby helping to elucidate the etiology of the obstruction and rule out neoplasms. This provides a direct basis for informed clinical decision-making regarding minimally invasive treatment of atypical, delayed-presentation duodenal obstruction.

Background:Video capsule endoscopy (VCE) is a noninvasive modality in the assessment among patients with very early onset inflammatory bowel disease (VEOIBD). Little is known about the application of VCE in this rare disorder. The aim of this study is to evaluate the features of patients with VEOIBD undergoing VCE. Methods:We retrospectively reviewed 37 VEOIBD patients who underwent VCE from five tertiary centers. Clinical data, including endoscopic findings and treatment were retrieved from medical records. Next generation sequencing was performed to confirm the monogenic defects. Results:During a decade, a total of 37 VEOIBD patients were retrospectively included from 5 specialist centers. The total number of VCE procedures performed was 58. The VCE was performed at an average age of 7.8±3.2 years. Twelve patients had undergone follow-up VCE. Next-generation sequencing confirmed the known monogenic inflammatory bowel disease (IBD) in 18 patients. Multiple ulcers, erosions and pseudo-polyps have been identified among patients with TNFAIP3, XIAP and PIK3CD mutations. No adverse effect including capsule retention or endoscopic delivery procedures related adverse effects were reported. Eighteen patients (48.6%) achieved clinical remission. Conclusions:This multicenter study showed the features of small bowel lesions among VEOIBD by VCE. Safety of VCE in VEOIBD patients have also been demonstrated.

Background & Aims: Alagille syndrome (ALGS) is an autosomal dominant disorder caused by JAG1 or NOTCH2 mutations and is the leading genetic cause of pediatric cholestatic liver disease. ALGS shows marked phenotypic heterogeneity and frequent misdiagnosis, with incompletely defined genotype–phenotype correlations. Although the ileal bile acid transporter (IBAT) inhibitors have revolutionized ALGS therapy, real-world data on Asian populations remain limited. We aimed to characterize the clinictreatment and features of Chinese pediatric ALGS patients, evaluate liver function changes with conventional treatment, and assess real-world maralixibat efficacy. Methods: This retrospective study included 19 children diagnosed with ALGS at Shenzhen Children’s Hospital (2011–2024). Clinical, genetic, and treatment data were analyzed, and comparisons were made between the JAG1 and NOTCH2 subgroups. Results: The median age at onset was 1.9 (0.1–3.7) years. Common features included cholestasis (63%), hepatobiliary involvement (84%), cardiac involvement (37%), skeletal involvement (31.6%), and renal anomalies (16%); no ocular defects were observed. JAG1 mutations accounted for 68.4% of the cases, and NOTCH2 for 31.6%. JAG1 mutations were clustered in exons 5 and 26, whereas NOTCH2 mutations were concentrated in exon 34. Patients with JAG1 variants had higher baseline ALT levels (P<0.05). Conventional therapy significantly reduced TBIL and DBIL levels at 1 month, with sustained improvement at 1 year (both P<0.05). Maralixibat showed benefits in one of the three patients. Conclusions: Chinese patients with ALGS exhibit distinct clinical and genetic characteristics. JAG1 is the major causative gene associated with more severe liver injury. Conventional and targeted IBAT therapies are effective in treating these conditions. Early genetic testing and personalized management can improve long-term outcomes.

Importance: Obesity and non-alcoholic fatty liver disease (NAFLD) guidelines recommend screening for NAFLD in children with obesity or overweight plus metabolic abnormalities. However, which metabolic factor is more closely associated with NAFLD in children with overweight or obesity remains unknown, and the risk of NAFLD in non-overweight children with metabolic abnormalities remains unclear. Objective: We aimed to explore the prevalence of NAFLD and its association with different combinations of weight status and metabolic abnormalities in children aged 6-18 years. Methods: Participants aged 6-18 years were recruited from the China Child and Adolescent NAFLD Study (CCANS). NAFLD was defined by ultrasonography or magnetic resonance imaging-proton density fat fraction (MRI-PDFF). Metabolic abnormalities include hypertension, hyperglycemia, hyperuricemia, high triglycerides (TG), low high-density lipoprotein cholesterol, and high low-density lipoprotein cholesterol. Multiple logistic regression models were used to assess the association of different combinations of weight statuses and metabolic abnormalities with NAFLD. Results: A total of 11 760 participants were included. The prevalence of NAFLD increased with increasing weight status (1.1%, 13.7%, and 39.8% among children with non-overweight, overweight, and obesity, respectively; P-for trend < 0.001). The prevalence of NAFLD in boys and girls with general obesity was 45.0% and 28.6%, respectively. The prevalence of NAFLD in boys and girls with central obesity was 51.3% and 35.6%, respectively. After adjusting for confounding risk factors, the models revealed that in non-overweight individuals, those with hyperglycemia (odds ratio [OR] = 7.46; 95% confidence interval [CI]: 2.39-23.26) or high TG levels (OR = 3.55; 95% CI: 1.39-9.06) had a significantly greater risk of NAFLD than those without. The odds ratio of NAFLD assessed in this study was greater in overweight individuals with hypertension, hyperuricemia, and high TG levels than in overweight individuals without metabolic abnormalities, with odds ratios ranging from 3.09 (95% CI: 1.24-7.67) to 4.48 (95% CI: 1.61-12.49). Interpretation: Non-overweight children with metabolic abnormalities might have an increased risk of NAFLD. These findings suggest that overweight and obesity should not be the sole criteria for NAFLD screening in children. In particular, more attention should be given to screening for NAFLD in non-overweight children with metabolic abnormalities, as well as in overweight children.

BackgroundFecal microbiota transplantation (FMT) shows promise for autism spectrum disorder (ASD) by modulating the gut-brain axis, but the optimal delivery route remains unknown. Our previous single-arm study suggested efficacy of nasojejunal FMT in children with moderate-to-severe ASD, yet could not exclude placebo effects or compare routes. This randomized controlled trial aims to determine the most effective and tolerable FMT administration route.MethodsThis single-center, randomized, triple-blind, double-dummy, placebo-controlled, three-arm parallel-group trial will enroll 75 children (aged 3–16 years) with moderate-to-severe ASD [Childhood Autism Rating Scale, Second Edition (CARS-2) ≥36]. Participants are randomized 1:1:1 to: (1) FMT via nasojejunal tube + sham colonoscopy (FMT-NJT); (2) active FMT via colonoscopy with transendoscopic enteral tube placement (first session) + two subsequent infusions via the indwelling tube + sham nasojejunal intubation (FMT-C); (3) placebo via both routes (sham procedures). Three FMT/placebo sessions (5 mL/kg, max 100 mL) are administered over 5 days. Primary outcome is change in CARS-2 score from baseline to Week 24. Secondary outcomes include changes in Social Responsiveness Scale, Autism Behavior Checklist, Gastrointestinal Symptom Rating Scale, Short Sensory Profile, Children's Sleep Habits Questionnaire, gut metagenomic profiles (baseline, Weeks 2,6,12,24,48), and adverse events.ResultsThis is a study protocol; no results are available.ConclusionsThis first head-to-head comparison of FMT routes in pediatric ASD will provide high-level evidence to guide treatment standardization, directly addressing the translational gap identified in our preliminary work.

Background:Autism spectrum disorder (ASD) is a neurodevelopmental condition affecting 0.7% of children globally, with 90% experiencing comorbid gastrointestinal (GI) symptoms. Fecal microbiota transplantation (FMT) may modulate ASD symptoms via the microbiota-gut-brain axis (MGBA). Methods:This open-label single-arm trial enrolls 30 children (2-12 years) with moderate-to-severe ASD, defined as a Childhood Autism Rating Scale (CARS) score of ≥36. Participants receive 3 nasojejunal FMTs (5 mL/kg) over 5 days. The primary outcomes are GI symptom improvement, assessed using the Gastrointestinal Symptom Rating Scale (GSRS), and ASD severity, assessed using the CARS. Secondary outcomes include social responsiveness (Social Responsiveness Scale, SRS), aberrant behaviors (Aberrant Behavior Checklist, ABC), and gut microbiota changes assessed by metagenomic next-generation sequencing (mNGS). Ethics and dissemination:Ethical approval obtained from Shenzhen Children's Hospital Ethics Committee. Results will be disseminated via peer-reviewed publications and conference presentations.Clinical Trial Registration: https://www.chictr.org.cn/showproj.html?proj=229136, identifier ChiCTR2400083998. Registered on 2024-05-08. Registered title: "Efficacy and safety of fecal microbiota transplantation in treatment of autism spectrum disorder: a prospective single-center intervention study".

This study aimed to assess the malnutrition risk of hospitalized children with digestive system diseases and provide evidence for clinical nutritional support. In this single-enter cross-sectional study, the modified pediatric malnutrition risk screening tool was used to assess the malnutrition risk of pediatric patients hospitalized for digestive system diseases from January 2024 to June 2024. The screening was carried out within 24 h after admission, and scores ≥4 and <4 were considered as high risk of malnutrition and non-high risk of malnutrition, respectively. We collected the data from all children, including age, gender, malnutrition risk, nutritional support, and clinical outcomes. SPSS software package (version 23.0) was used for data processing. A total of 1,200 children aged 1 month to 18 years were included in this study. The incidence of malnutrition risk in all hospitalized children was 53.17%, and the percentage of high malnutrition risk was 13.67%. There was a significant difference in the incidence of high malnutrition risk between different diseases (P < 0.01). The difference in nutritional support rate (P < 0.05) and outcomes (P < 0.05) was also significant in patients with different degrees of malnutrition risk. Timely, standardized, and comprehensive nutritional assessment is of crucial importance for reasonable nutritional interventions to improve clinical outcomes in children with high malnutrition risk.

Inflammatory bowel disease (IBD) presents significant clinical challenges due to its multifaceted pathogenesis and the limited efficacy of existing therapies. This study investigates the therapeutic potential of Cu–Zn@HA bimetallic nanozymes for the treatment of colitis. Through in vivo experiments, we demonstrated that these nanozymes exhibit sustained retention in the colon, facilitating effective modulation of gut microbiota composition and diversity. Notably, Cu–Zn@HA nanozymes significantly enhanced α-diversity and induced distinct alterations in microbial community structure across treatment groups. While no marked differences were observed in the Firmicutes/Bacteroidetes ratio, our biomarker analyses indicated critical shifts in bacterial populations associated with gut health and inflammatory responses. Additionally, Cu–Zn@HA nanozymes effectively scavenged reactive oxygen species (ROS) and promoted macrophage polarization, contributing to an anti-inflammatory microenvironment. Importantly, our studies confirmed the excellent safety profile of these nanozymes. Collectively, these findings underscore the promising role of Cu–Zn@HA bimetallic nanozymes as a novel therapeutic strategy for IBD, paving the way for future investigations into their clinical efficacy and safety.

Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most prevalent chronic liver condition in adolescents. The triglyceride-glucose (TyG) index, a surrogate marker of insulin resistance, has shown promise in adult MAFLD detection but requires pediatric-specific validation, particularly when combined with anthropometric measures. This study investigated the association between modified TyG indices and MAFLD, and evaluated their predictive value in adolescents. This cross-sectional study analyzed data from 532 adolescents (12–18 years) in the 2017–2020 National Health and Nutrition Examination Survey (NHANES) with complete records. MAFLD diagnosis was based on transient elastography plus metabolic criteria. The investigators employed multivariate linear regression and restricted cubic splines (RCS) to examine linear and nonlinear relationships between modified TyG indices and CAP values. Subgroup analyses were stratified by obesity status, and sensitivity analyses were performed on the NAFLD cohort (n = 527). Receiver operating characteristic (ROC) curve analysis, using Youden's index, evaluated the predictive performance of TyG indices for MAFLD identification. Among 130 MAFLD adolescents (vs 402 controls), modified TyG indices demonstrated significantly stronger associations with CAP in fully adjusted models compared to the original TyG index. TyG-WC showed the highest diagnostic accuracy (AUC = 0.923, 95

Periodontitis is a chronic inflammatory disease affecting the supporting tissues of the teeth and has emerged as a global public health issue. Current therapies primarily address pathogenic factors and alleviate symptoms, with limited options available for complete restoration and reconstruction of already absorbed periodontal bone tissue. In this study, we developed a nanotherapeutic strategy utilizing fusion nanovesicles (FVs) to modulate the inflammatory microenvironment and create a regenerative niche for periodontal ligament stem cells (PDLSCs), which play a crucial role in periodontal tissue repair. The FVs are composed of Scutellaria baicalensis nanovesicles (SBNVs) with anti-Porphyromonas gingivalis (P. gingivalis) and anti-inflammatory properties, combined with PDLSC membrane-derived nanovesicles genetically engineered to express TNFR1. These FVs preserved the biological activity of SBNVs and the immunomodulatory function of PDLSCs. Additionally, FVs effectively captured and cleared TNF-α from the microenvironment through TNFR1. Moreover, FVs alleviated the inflammatory response of PDLSCs induced by P. gingivalis-LPS (Pg-LPS) and TNF-α, restoring their proliferation, migration, and osteogenic differentiation capabilities. Hence, this nanotherapeutic strategy holds great potential for treating periodontitis.

Parabacteroides distasonis is a prevalent human gut bacterium. Here, we report the draft genome of P. distasonis SZCHProba001 isolated from a 6-year-old boy's feces. The 5.03 Mb assembly (102 contigs) contains 4,099 predicted proteins and 76 RNAs. This resource aids research into P. distasonis' role in pediatric gut health.

The newly proposed metabolic-associated fatty liver disease (MAFLD) definition better reflects the metabolic pathogenesis shared with non-alcoholic fatty liver disease (NAFLD), though with incomplete diagnostic overlap; this study systematically compares their prevalence and risk profiles in U.S. adolescents to inform optimal clinical management strategies. This cross-sectional study analyzed participants with complete survey data from the 2017–2020 cycle of the National Health and Nutrition Examination Survey (NHANES), identifying and comparing 532 MAFLD cases and 527 NAFLD cases through comprehensive prevalence assessment, detailed clinical characterization, regression for variable selection, and multivariate logistic regression analysis of independent risk factor associations. MAFLD prevalence was 22.8

Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is an autosomal recessive disorder with heterogeneous clinical manifestations. This study aimed to characterize the clinical, biochemical, and genetic spectrum of NICCD and evaluate treatment outcomes. This retrospective cohort study analyzed molecularly confirmed cases of NICCD admitted to Shenzhen Children’s Hospital between March 2019 and April 2023. Comprehensive clinical data were extracted from electronic records and analyzed using descriptive statistical methods. The cohort (n = 15) demonstrated universal jaundice (100

Here, we report the draft genome sequence of Mediterraneibacter faecis SZCH001, isolated from a fecal sample of an autistic child. The bacterial genome was sequenced using Illumina technology on a Novaseq 6000 platform. The assembled genome of M. faecis comprises 3,423,666 base pairs with a G+C content of 40.27%.

IntroductionCurrent research underscores the critical role of the gut-skin axis in inflammatory skin disorders such as psoriasis, with growing interest in the therapeutic application of probiotics. Despite this promise, the specific mechanisms and bioactive compounds through which probiotics exert their effects remain poorly characterized. In this study, we aimed to systematically evaluate the therapeutic potential of Lactobacillus plantarum (Lp)-derived bioactive fractions in psoriasis, with a particular focus on identifying key anti-inflammatory and immunomodulatory metabolites.MethodsThe microbiome characteristics of psoriasis were analyzed through open microflora data mining and bibliometrics, and the probiotics with potential therapeutic effects were identified. Four bioactive fractions from L. plantarum were extracted and characterized. CCK-8, qPCR, and flow cytometry were used to evaluate the effects of four bioactive components on oxidative stress in keratinocytes and inflammatory responses in macrophages. Metabolomics was used to analyze the metabolic profiles of bioactive components with anti-inflammatory and antioxidant properties, and to screen and identify the main metabolite that play a role. To evaluate the efficacy and safety of bioactive components in the treatment of IMQ-induced psoriasis in mice.ResultsA common feature of downregulation of Lactobacillus abundance was shown in patients with four inflammatory skin diseases including psoriasis. Four bioactive fractions, namely cytoplastic membrane vesicles (CMVs), bacterial lysate supernatant (BL-S), bacterial lysate precipitate (BL-P) and cell-free fermentation supernatant (CFS), were extracted from L. plantarum ATCC BAA-793, and CMVs were identified as having typical extracellular vesicles. In efficacy evaluation, CMVs and BL-S significantly reduced the mRNA levels of inflammatory factors in macrophages and the ROS levels of inflamed keratinocytes, among which CMVs had a more significant anti-inflammatory effect and had a unique inhibitory effect on M1 polarization of macrophages. Metabolomics revealed significant differences in metabolite profiles between CMVs and BL-S, and AEA enriched in both played anti-inflammatory, antioxidant and inhibitory roles in macrophage M1 polarization. In IMQ-induced psoriasis mouse models, CMVs demonstrated superior effects over BL-S in anti-hyperkeratosis, inhibiting inflammatory factor production, and down-regulating the proportion of M1 macrophages in skin and spleen. Both showed good biosafety in vivo.DiscussionThis study demonstrates that L. plantarum-derived CMVs, enriched with AEA, ameliorate psoriasis through multi-faceted mechanisms including anti-inflammation, antioxidative stress reduction, and reprogramming of macrophage polarization. These findings not only position bacterial nanovesicles as a novel cell-free therapeutic strategy for inflammatory skin diseases but also establish a functional screening platform for precision microbiome-based interventions.

Abnormal SUMOylation is implicated in non-alcoholic fatty liver disease (NAFLD) progression. Forkhead box protein A1 (FoxA1) has been shown to protect liver from steatosis, which was down-regulated in NAFLD. This study elucidated the role of FoxA1 deSUMOylation in NAFLD. NAFLD models were established in high-fat diet (HFD)-induced mice and palmitate acid (PAL)-treated hepatocytes. Hepatic steatosis was evaluated by biochemical and histological methods. Lipid droplet formation was determined by BODIPY and Oil red O staining. Target molecule levels were analyzed by RT-qPCR, Western blotting, and immunohistochemistry staining. SUMOylation of FoxA1 was determined by Ni-NTA pull-down assay and SUMOylation assay Ultra Kit. Protein interaction and ubiquitination were detected by Co-IP. Gene transcription was assessed by ChIP and dual luciferase reporter assays. Liver FoxA1 knockout mice developed severe liver steatosis, which could be ameliorated by sirtuin 6 (Sirt6) overexpression. Nutritional stresses reduced Sumo2/3-mediated FoxA1 SUMOylation at lysine residue K6, which promoted lipid droplet formation by repressing fatty acid β-oxidation. Moreover, Sirt6 was a target gene of FoxA1, and Sirt6 transcription activity was restrained by deSUMOylation of FoxA1 at site K6. Furthermore, nutritional stresses-induced deSUMOylation of FoxA1 promoted the ubiquitination and degradation of FoxA1 with assistance of murine double minute 2 (Mdm2). Finally, activating FoxA1 SUMOylation delayed the progression of NAFLD in mice. DeSUMOylation of FoxA1 at K6 promotes FoxA1 degradation and then inhibits Sirt6 transcription, thereby suppressing fatty acid β-oxidation and facilitating NAFLD development. Our findings suggest that FoxA1 SUMOylation activation might be a promising therapeutic strategy for NAFLD.

BackgroundMetabolic dysfunction-associated steatohepatitis (MASH) is characterized by liver inflammation and damage caused by a buildup of fat in the liver. Hepatitis C, caused by hepatitis C virus (HCV), is a disease that can lead to liver cirrhosis, liver cancer, and liver failure. MASH and hepatitis C are the common causes of liver cirrhosis and hepatocellular carcinoma. Several studies have shown that hepatic steatosis is also a common histological feature of liver in HCV infected patients. However, the common molecular basis for MASH and hepatitis C remains poorly understood.MethodsFirstly, differentially expressed genes (DEGs) for MASH and hepatitis C were extracted from the GSE89632, GSE164760 and GSE14323 datasets. Subsequently, the common DEGs shared among these datasets were determined using the Venn diagram. Next, a protein-protein interaction (PPI) network was constructed based on the common DEGs and the hub genes were extracted. Then, gene ontology (GO) and pathway analysis of the common DEGs were performed. Furthermore, transcription factors (TFs) and miRNAs regulatory networks were constructed, and drug candidates were identified. After the MASH and hepatitis C cell model was treated with predicted drug, the expression levels of the signature genes were measured by qRT-PCR and ELISA.Results866 common DEGs were identified in MASH and hepatitis C. The GO analysis showed that the most significantly enriched biological process of the DEGs was the positive regulation of cytokine production. 10 hub genes, including STAT1, CCL2, ITGAM, PTPRC, CXCL9, IL15, SELL, VCAM1, TLR4 and CCL5, were selected from the PPI network. By constructing the TF-gene and miRNA-gene network, most prominent TFs and miRNAs were screened out. Potential drugs screening shows that Budesonide and Dinoprostone may benefit patients, and cellular experiments showed that Budesonide effectively inhibited the expression of genes related to glycolipid metabolism, fibrosis, and inflammatory factors.ConclusionWe extracted 10 hub genes between MASH and hepatitis C, and performed a series of analyses on the genes. Molecular docking and in vitro studies have revealed that Budesonide can effectively suppress the progression of MASH and hepatitis C. This study can provide novel insights into the potential drug targets and biomarkers for MASH and hepatitis C.

Background: Therapeutic effect of traditional medicines for nonalcoholic fatty liver disease (NAFLD) is far from satisfactory. Tea has been shown to have efficacy in preventing NAFLD. We hypothesized that tea derived extracellular vesicles (TDEVs) may attenuate NAFLD. Methods: Extracellular vesicles (EVs) were isolated from fresh tea. High Performance Liquid Chromatography (HPLC) was used to detect the epigallocatechin-3-gallate (EGCG)in TDEVs. Oleic acid-induced HepG2 cells were treated with different doses of TDEVs. Oil red O staining and fluorescent staining were used to analyze TDEVs efficacy in NAFLD HepG2 cell model. Enzyme‑linked immunosorbent assay (ELISA) was applied to evaluate the levels of triglycerides (TG) and interleukin 6 (IL-6). Q-PCR technique was used to detect the mRNA expressions of MTTP, and Western Blotting was applied to evaluate their protein expressions. Bisulfite genomic sequencing was used to analyze the level of DNA methylation within the promoter of MTTP gene. Results: The concentrations of EGCG in TDEVs was 1.031 ± 0.044 mg/ml, equivalent to 5.6 mg/100 g/FW. Oil red O staining and fluorescent staining demonstrated TDEVs absorbed by HepG2 cells contributed to oil droplets decomposition and a consequential decrease in TG and IL-6 levels. Q-PCR and Western Blotting showed an upregulation in MTTP gene expression by TDEVs. Bisulfite genomic sequencing analysis revealed a reduction in the methylation level of MTTP gene in TDEVs groups. Conclusion: The results of this study indicated that TDEVs attenuated NAFLD via reducing TG level by inhibition of MTTP gene methylation in NAFLD cell model.

AbstractUlcerative colitis (UC) belongs to chronic inflammatory disease with a relapsing characterization. Conventional oral drugs of UC are restricted in clinical by premature degradation in the gastrointestinal tract, modest efficacy, and adverse effects. CX5461 can treat autoimmune disease, immunological rejection, and vascular inflammation. However, low solubility, intravenous administration, and non-inflammatory targeting limited its clinical application. Herein, this work aims to develop Sophora Flavescens-derived exosomes-like nanovesicles carrying CX5461 (SFELNVs@CX5461) for efficient CX5461 oral delivery for UC therapy. We identified SFELNVs as nano-diameter (80 nm) with negative zeta potential (-32mV). Cellular uptake has shown that SFELNVs were targeted uptake by macrophages, thus increasing drug concentration. Additionally, oral SFELNVs@CX5461 exhibited good safety and stability, as well as inflammation-targeting ability in the gastrointestinal tract of dextran sodium sulfate (DSS)-induced colitis mice. In vivo, oral administration of SFELNVs and CX5461 could relieve mice colitis. More importantly, combined SFELNVs and CX5461 alleviated mice colitis by inhibiting pro-inflammatory factors (TNF-α, IL-1β, and IL-6) expression and promoting M2 macrophage polarization. Furthermore, SFELNVs promoted M2 polarization by miR4371c using miRNA sequencing. Our results suggest that SFELNVs@CX5461 represents a novel orally therapeutic drug that can ameliorate colitis, and a promising targeting strategy for safe UC therapy.