Symptoms Of Colitis Research Articles

Effect of Artemisia vulgaris Hydro-Alcoholic Extract on Oxidative Stress and Inflammatory Damages in a Rat Model of Experimental Colitis

Background: Herbal medicines can be used as a possible therapeutic agent in inflammatory diseases. Objectives: This study aimed to determine the effect of Artemisia vulgaris (AV) hydro-alcoholic extract on oxidative stress and inflammatory damage in an experimental rat model of colitis. Methods: Thirty male Sprague-Dawley rats were randomly divided into 6 groups: Control, colitis, sulfasalazine, AV50, AV100, and AV200. The animals of the AV groups were treated with the hydro-alcoholic extract of A. vulgaris via gavage for 72 h. Body weight was measured at the beginning and end of the experiment. In the end, serum levels of malondialdehyde (MDA) as a lipid peroxidation marker, antioxidants such as glutathione (GSH), superoxide dismutase (SOD) activity, serum tumor necrosis factor-α (TNF-α), and nitric oxide (NO) levels as inflammatory biomarkers were measured. Macroscopic and microscopic damage in the rat's colon was also examined in histological studies. Results: The A. vulgaris extract treatment dose-dependently improved colonic injury (P < 0.001 to P < 0.05) and body weight (P < 0.001) in colitis rats. Moreover, it enhanced SOD activity and GSH levels (P < 0.001) and reduced serum MDA, TNF-α, and NO levels (P < 0.001 to P < 0.01) in the rats with colitis. Conclusions: Treatment with A. vulgaris could mitigate ulcerative colitis (UC) symptoms, which is probably attributed to its antioxidant and anti-inflammatory properties.

Effect of Extracelluar Vesicles Derived from Akkermansia muciniphila on Intestinal Barrier in Colitis Mice.

Inflammatory bowel disease (IBD) is a chronic and recurrent disease. It has been observed that the incidence and prevalence of IBD are increasing, which consequently raises the risk of developing colon cancer. Recently, the regulation of the intestinal barrier by probiotics has become an effective treatment for colitis. Akkermansia muciniphila-derived extracellular vesicles (Akk EVs) are nano-vesicles that contain multiple bioactive macromolecules with the potential to modulate the intestinal barrier. In this study, we used ultrafiltration in conjunction with high-speed centrifugation to extract Akk EVs. A lipopolysaccharide (LPS)-induced RAW264.7 cell model was established to assess the anti-inflammatory effects of Akk EVs. It was found that Akk EVs were able to be absorbed by RAW264.7 cells and significantly reduce the expression of nitric oxide (NO), TNF-α, and IL-1β (p < 0.05). We explored the preventative effects on colitis and the regulating effects on the intestinal barrier using a mouse colitis model caused by dextran sulfate sodium (DSS). The findings demonstrated that Akk EVs effectively prevented colitis symptoms and reduced colonic tissue injury. Additionally, Akk EVs significantly enhanced the effectiveness of the intestinal barrier by elevating the expression of MUC2 (0.53 ± 0.07), improving mucus integrity, and reducing intestinal permeability (p < 0.05). Moreover, Akk EVs increased the proportion of the beneficial bacteria Firmicutes (33.01 ± 0.09%) and downregulated the proportion of the harmful bacteria Proteobacteria (0.32 ± 0.27%). These findings suggest that Akk EVs possess the ability to regulate immune responses, protect intestinal barriers, and modulate the gut microbiota. The research presents a potential intervention approach for Akk EVs to prevent colitis.

The Frequency and Impact of Self-Imposed Elimination Diets on the Nutritional Status and Clinical Course of Disease in Children with Inflammatory Bowel Disease.

From the patients' perspective, diet has a relevant role in triggering symptoms of inflammatory bowel disease (IBD). There is a lack of prospective studies regarding the diet of children with IBD. The aim of this study was to assess the frequency and impact of self-imposed elimination diets on the nutritional status and clinical course of disease in the pediatric population. This was a prospective case-control study that included newly diagnosed patients with IBD and healthy controls (age/sex-matched peers and siblings) over a one-year period. The participants were examined in three categories: (1) anthropometric data and nutritional status; (2) dietary intake, as obtained by a Food Frequency Questionnaire (FFQ); and (3) dietary beliefs and elimination diets, as obtained by a structured questionnaire. Overall, one-hundred and thirty-seven participants were included (twenty-eight with Crohn's disease, sixteen with ulcerative colitis, three with IBD-unclassified, and seventy healthy controls). Only 15% of patients followed the self-imposed elimination diet upon the diagnosis, which increased to 47.6% by the end of the follow-up. The elimination diet did not influence the nutritional status and quality of the diet. Self-imposed elimination diets were not a risk factor for disease relapse. Most of the patients received nutritional counseling during the follow-up. The number of patients following self-imposed elimination diets had increased during the disease course but with no influence on nutritional status or relapse risk.

TNF-α Inhibitor-Induced Psoriasis and Psoriatic Alopecia in Adolescent with Ulcerative Colitis: Clinical Case

Background. Genetically engineered biological therapy has revolutionized the treatment of many chronic inflammatory diseases. It often allows to achieve significant clinical effect and improve the patient's quality of life. However, sometimes it leads to adverse events, and physicians encounter them more often. One of such side effects is paradoxical psoriasis (PP) that can be revealed during the therapy with tumor necrosis factor alpha (TNF-α) inhibitors. PP is the debut or exacerbation of pre-existing psoriasis.Clinical case description. Patient A., 17 years old, has suffered from ulcerative colitis since 2020; biological therapy with infliximab has been initiated in March 2022. Numerous rashes were revealed, as well as development of confluent alopecia foci on the background of scalp psoriatic damage, during the next hospitalization in December 2022. The patient was examined by dermatologist; diagnosis of PP was established according to the clinical picture and medical history. Skin rashes progressed and ulcerative colitis worsened (diarrheal syndrome, fecal calprotectin levels increased up to 526 μg/g) after cessation of infliximab therapy. Biological therapy with the inhibitor IL-12/23 (ustekinumab) was initiated due to the aggressive cutaneous pathological process and the aggravation of inflammatory bowel disease (IBD) symptoms. The gradual regression of rashes with the restoration of scalp hair growth and ulcerative colitis clinical and laboratory remission were noted during the treatment.Conclusion. PP is a rare complication that develops during therapy with TNF-α inhibitors, and it is most often observed in patients with IBD. In our case there was aggressive course of psoriasis with severe scalp lesion and hair loss (it is specific type of lesion in such patients). The ustekinumab, inhibitor IL-12/23, treatment efficacy correlates with the literature data on this drug successful use in both nosologies. Ustekinumab can be a first-line therapy in such pediatric patients. This clinical case is the first case in the Russian literature on effective management of PP and ulcerative colitis with ustekinumab in children.

The transcription factor ELF4 alleviates inflammatory bowel disease by activating IL1RN transcription, suppressing inflammatory TH17 cell activity, and inducing macrophage M2 polarization.

Inflammatory bowel disease (IBD) is a chronic immune-mediated disorder affecting millions worldwide. Due to the complexity of its pathogenesis, the treatment options for IBD are limited. This study focuses on ELF4, a member of the ETS transcription factor family, as a target to elucidate its role in IBD and investigate its mechanism of action in alleviating IBD symptoms by activating IL1RN transcription to suppress the activity of inflammatory TH17 cells. Using the GEO database, this study examined LPS-induced intestinal inflammatory genes and their regulation mechanisms. We examined the colon length of LPS-treated mice and derived the Disease Activity Index (DAI). H&E staining, ELISA, and flow cytometry were used to detect mice colon tissue damage, inflammatory factor levels in mouse serum, mouse macrophage types and inflammatory TH17 cell activity. RT-qPCR and Western blot detected ELF4, IL1RN, M1, and M2 polarization markers. In Vitro, using dual-luciferase and ChIP assays, we tested mouse bone marrow-derived macrophages (BMDMs) and mouse intestinal epithelial cells for IL1RN promoter activity and ELF4 enrichment. Bioinformatics showed that LPS-induced colitis animals have reduced ELF4 expression in their colon tissue. In vivo tests confirmed reduced ELF4 expression in mice with LPS-induced colitis. ELF4 overexpression reduced mouse intestinal inflammation. ELF4 activated IL1RN transcription in bioinformatics and in vitro tests. ELF4 promoted IL1RN transcription and macrophage M2 polarization to limit intestinal epithelial cell death and inflammation and reduce mouse intestinal inflammation in vitro. ELF4 also reduced the Th17/Treg ratio by increasing IL1RN transcription. ELF4 activates IL1RN transcription, suppresses inflammatory TH17 cells, and induces macrophage M2 polarization to treat IBD.

A novel Sagittaria sagittifolia L. polysaccharides mitigate DSS-induced colitis via modulation of gut microbiota and MAPK/NF-κB signaling pathways

Sagittaria sagittifolia L. polysaccharides possess anti-inflammatory, antioxidant, and immune-modulatory properties. In this study, we identified a novel S. sagittifolia L. polysaccharide, named PSSP-1, and evaluated its potential in alleviating dextran sulfate sodium (DSS)-induced colitis in a mouse model. The results demonstrated that administration of PSSP-1 at doses of 100, 200, and 400 mg/kg·bw significantly reduced the disease activity index (DAI) and suppressed the expression of inflammatory cytokines in UC mice. Furthermore, PSSP-1 treatment upregulated the expression levels of claudin-1, occludin, and ZO-1, and promoted the diversity and abundance of beneficial gut microbiota, including Lactobacillus and Candidatus_Saccharimonas, while reducing the levels of Bacteroidetes and Verrucomicrobiota. Particularly, the Lactobacillus_johnsonii species may play a potentially significant role in modulating colitis. Subsequently, there was a significant increase in the levels of short-chain fatty acids (SCFAs). Additionally, the correlation analyses revealed positive associations between PSSP-1 supplementation and Nitrosospira and Dialister, which are implicated in gut inflammation. Mechanistically, PSSP-1 intervention inhibited the protein phosphorylation of key molecules in the MAPK and NF-κB signaling pathways. Collectively, these findings suggest that PSSP-1 mitigates colitis symptoms by repairing the intestinal barrier, promoting microbial metabolism, and regulating the gut microbiota-MAPK/NF-κB signaling pathways.

Mechanosignaling YAP/TAZ-TEAD Axis Regulates the Immunomodulatory Properties of Mesenchymal Stem Cells.

Mesenchymal stem cells (MSCs) have gained significant attention in cell therapies due to their multipotency and immunomodulatory capacities. The transcriptional co-activators YAP/TAZ, central to the mechanotransduction system in MSCs, dominantly direct MSCs lineage commitment. However, their role in immunomodulation remains elusive. Accordingly, this present study aimed to investigate the role of mechanotransducer YAP/TAZ and their binding target transcriptional factor, TEAD, in the immunomodulatory capacities of human bone marrow-derived MSCs. Reducing YAP/TAZ activity by altering the matrix stiffness, disrupting the F-actin integrity with chemical inhibitors, or using siRNAs increased the expression of immunomodulatory genes, such as TSG-6 and IDO, upon TNF-α stimulation. Similarly, transfection of TEAD siRNA also increased the immunomodulatory capacities in MSCs. RNA-seq analysis and inhibition assays demonstrated that the immunomodulatory capacities caused by YAP/TAZ-TEAD axis disruption were due to the NF-κB signaling pathway activation. Then, we also evaluated the in vivo anti-inflammatory efficacy of MSCs in a dextran sulfate sodium (DSS)-induced mice colitis model. The administration of human MSCs transfected with TEAD siRNA, which exhibited enhanced immunomodulatory properties in vitro, significantly ameliorated inflammatory bowel disease symptoms, such as body weight loss and acute colon inflammation, in the DSS-induced mice colitis model. Our findings underscore the mechanosignaling YAP/TAZ-TEAD axis as a regulator of MSCs immunomodulation. Targeting these signaling pathways could herald promising MSCs-based therapies for immune disorders.

Discovery of a novel GPR35 agonist with high and equipotent species potency for oral treatment of IBD

The G protein-coupled receptor 35 (GPR35) has been identified as a potential target in the treatment of inflammatory bowel disease (IBD). However, the lack of high and equipotent agonists on both human and mouse GPR35 has limited the in vivo study of GPR35 agonists in mouse models of IBD. In this study, structural modifications to lodoxamide provides a series of high and equivalent agonists on human, mouse, and rat GPR35. These molecules eliminate the species selectivity of human to mouse and rat orthologs that have been prevalent with GPR35 agonists including lodoxamide. The cLogP properties are also optimized to make the compounds more obedient to drug-like rules, yielding compound 4b (cLogP = 2.41), which activates human, mouse or rat GPR35 with EC50 values of 76.0, 63.7 and 77.8 nM, respectively. Oral administration of compound 4b at 20 mg/kg alleviates clinical symptoms of DSS-induced IBD in mice, and is slightly more effective than 5-ASA at 200 mg/kg. In summary, it can serve as a new start point for exploiting more potent GPR35 agonists without species differences for the treatment of IBD, and warrants further study.

A novel causative role of imbalanced kynurenine pathway in ulcerative colitis: Upregulation of KMO and KYNU promotes intestinal inflammation

The kynurenine pathway (KP) is the principal metabolic route for the essential amino acid tryptophan (TRP). Recent advances have highlighted a pivotal role for several KP metabolites in inflammatory diseases, including ulcerative colitis (UC). However, the alterations of KP enzymes and their functional impact in UC remain poorly defined. Here, we focused on kynurenine 3-monooxygenase (KMO) and kynureninase (KYNU), which serve as critical branching enzymes in the KP. We observed that dextran sodium sulfate (DSS)-induced colitis mice exhibited disturbed TRP metabolism along with KMO and KYNU upregulated. In patients with active UC, both the expression of KMO and KYNU were positively correlated with inflammatory factors TNF-α and IL-1β. Pharmacological blockade of KMO or genetic silencing of KYNU suppressed IL-1β-triggered proinflammatory cytokines expression in intestinal epithelial cells. Furthermore, blockage of KMO by selective inhibitor Ro 61-8048 alleviated the symptoms of DSS-induced colitis in mice, accompanied by an expanded NAD+ pool and redox balance restoration. The protective role of Ro 61-8048 may be partly due to its effect on KP regulation, particularly in enhancing kynurenic acid production. In summary, our study provides new evidence for the proinflammatory property of KMO and KYNU in intestinal inflammation, hinting at a promising therapeutic approach in UC through targeting these enzymes.

Disrupting endogenous retroelements with a reverse transcriptase inhibitor alleviates DSS-induced colitis in mice

Endogenous retroelements play vital roles in sustaining immune homeostasis. Activation of endogenous retroelements can trigger cGAS/STING pathway and downstream pro-inflammatory cytokine production. Activated macrophages (M1), which can be induced by pro-inflammatory cytokines, are involved in the development of colitis. Here we aimed to determine whether a retrovirus reverse transcriptase inhibitor azidothymidine (AZT) could influence M1 macrophage polarization and rescue colitis by inhibiting the reverse transcription of murine endogenous retroelements. A dextran sodium sulfate salt (DSS)-induced colitis mouse model (male C57BL/6N) and a lipopolysaccharides-treated RAW264.7 cell line were used to evaluate the protective role of AZT in colitis alleviation. An upregulated expression of endogenous retroelements was first detected in both the colons of the mice with colitis and the lipopolysaccharides-stimulated M1 cells, and treatment with AZT significantly decreased the expression. Meanwhile, a downregulation of cGAS/STING/NF-κB pathway and pro-inflammatory cytokines that induce M1 macrophage polarization was also observed in AZT-treated colitis or M1 groups. Moreover, the symptoms of DSS-induced colitis could be significantly alleviated by AZT. In summary, the endogenous retroelement inhibitor AZT could rescue the DSS-induced colitis possibly via blocking M1 macrophage polarization through cGAS/STING/NF-κB pro-inflammatory pathway. Thus, a pharmacological blockade of endogenous retroelements would be a new strategy for clinical therapy of colitis.

Inhibition of α2,6-sialyltransferase relieves symptoms of ulcerative colitis by regulating Th17 cells polarization

Ulcerative colitis (UC) is a chronic, relapsing inflammatory disease that affects human intestines. Immune imbalance is one of the important factors inducing UC. After the activation of CD4+ T cells, pro-inflammatory cytokines are produced to induce colonic inflammation. α2,6-Sialylation, catalyzed by α2,6-sialyltransferase (ST6GAL1), affects the proliferation, activation, and T cell receptor (TCR) signaling of CD4+ T cells, but its role in CD4+ T cell polarization, regulation of Th17 / Treg balance, and its role in UC are still unclear. We found the number of CD4+ T and Th17 cells increased in colonic tissue with UC. The level of α2,6-sialylation of CD4+ T cells in patients with UC was significantly increased. De-α2,6-sialylation significantly reduced the symptoms of UC in rats. ST6GAL1 gene knockout inhibited the polarization of CD4+ T cells to Th17 cells, and promoted the polarization of CD4+ T cells to Treg cells. ST6GAL1 knockout significantly inhibited the IL-17 signaling pathway in CD4+ T cells and inhibited the secretion of pro-inflammatory cytokine IL-17a. ST6GAL1 and IL-17a are highly expressed in patients with UC, and there is a positive correlation between them. In conclusion, reduced α2,6-sialylation inhibits the polarization of CD4+ T cells to Th17 cells, inhibits IL-17a signaling pathway and reduces the level of pro-inflammatory cytokine IL-17a to alleviate the symptoms of UC, which is a potential novel target for the clinical treatment of UC.

Antimicrobial resistance profiles of salmonella spp. and escherichia coli isolated from fresh nile tilapia (oreochromis niloticus) fish marketed for human consumption

BackgroundSalmonella spp. and pathogenic strains of Escherichia coli are among the major foodborne zoonotic pathogens. These bacterial pathogens cause human illnesses characterized by hemorrhagic colitis, vomiting, nausea, and other agent-related symptoms. The increasing occurrence of antimicrobial resistance in these pathogens is also a serious public health concern globally. Regular surveillance of phenotypes and genotypes of Salmonella spp. and Escherichia coli from animal-derived foods is necessary for effective reduction and control of these foodborne pathogens. This study was conducted to assess the occurrence, antimicrobial resistance, virulence genes and genetic diversity of Salmonella spp. and E. coli isolates from fresh Nile tilapia obtained from retail markets in Nairobi, Kenya.MethodsA total of 68 fresh Nile tilapia fish samples were collected from retail markets and used for isolation of Salmonella spp. and E. coli. Antimicrobial susceptibilities of the isolates weretested by Kirby-Bauer agar disc diffusion method. According to the antimicrobial resistance profiles, the multi-drug resistant isolates were identified by 16 S rRNA sequencing and phylogenetic analysis using the Bayesian inference method. The MDR Salmonella spp. and E. coli isolates were subjected to PCR-based screening for the detection virulence and antibiotic resistance genes.ResultsThe prevalence of contamination of the fish samples with Salmonella spp. and E.coli was 26.47% and 35.29% respectively. Overall phenotypic resistance among the Salmonella spp. ranged from 5.5% for ceftazidime, chloramphenicol, meropenem, nitrofurantoin and streptomycin and 22.2% for penicillin-G. For E. coli phenotypic resistance ranged from 4.2% for ceftazidime and chloramphenicol and 25% for rifampicin. Multi-drug resistance was observed in three Salmonella spp. and two E. coli isolates. Results of 16 S rRNA sequences, sequence alignment and phylogenic trees confirmed the identified MDR isolates as S. typhymurium WES-09, S. typhymurium MAK-22, S. typhimurium EMB-32 and E. coli MAK-26 and E. coli LAN-35. The presence of antibiotic-resistance genes belonging to β-lactamases, tetracycline, sulfonamide, trimethoprim and aminoglycosides-resistant genes were detected in all the identified MDR isolates.ConclusionsThe findings from this study indicate that Nile tilapia (Oreochromis niloticus) sold in retail markets can acts as reservoirs of Salmonella spp. and E. coli pathogens linked to human disease, some of which were multidrug resistance to critically important antimicrobials. Both microorganisms are of zoonotic significance and represent a significant public health risk to the society.

Phenolics from Dendrobium officinale Leaf Ameliorate Dextran Sulfate Sodium-Induced Chronic Colitis by Regulating Gut Microbiota and Intestinal Barrier.

The increasing incidence of colitis and the side effects of its therapeutic drugs have led to the search for compounds of natural origin, including phenolics, as new treatments for colitis. In this study, the potential mechanism of Dendrobium officinale leaf phenolics (DOP) on the relief of dextran sulfate sodium (DSS)-induced colitis was explored. The results showed that DOP treatment for 36 days reduced the symptoms of colitis caused by DSS, including reduction of the disease activity index and alleviation of colonic tissue damage. In addition, DOP downregulated the expression of key proteins of the TLR4/NF-κB signaling pathway and reduced the production of inflammatory cytokines. Furthermore, DOP could enhance the expression of tight junction proteins including ZO-1, Occludin, and Claudin-1 to restore intestinal mucosal barrier function. DOP also effectively regulates disordered intestinal flora and enhances the production of short-chain fatty acids, which is also beneficial in modulating gut internal environmental homeostasis, inhibiting inflammation, and restoring the intestinal barrier. These findings indicated that DOP can ameliorate DSS-induced chronic colitis by regulating gut microbiota, intestinal barrier, and inflammation, and it is a promising ingredient from D. officinale.

Quinoa protein and its hydrolysate ameliorated DSS-induced colitis in mice by modulating intestinal microbiota and inhibiting inflammatory response

The objective of this study was to investigate the protective effects of quinoa protein (QPro) and its derived peptides (QPep) in dextran sulfate sodium (DSS)-induced colitis in mice. The results demonstrated that oral administration of QPro and QPep significantly alleviated colitis symptoms, including diarrhea, abdominal pain, bloody stools, weight loss, as well as reduced colonic shortening, inflammatory factor release, and intestinal barrier injury. Short-chain fatty acids (SCFAs) production rose as QPro and QPep modulated the composition of the intestinal microbiota. Western blotting results revealed that QPro and QPep also suppressed TLR4 levels and inhibited IκB-α and NF-κB phosphorylation in colon tissue, implying that the TLR4/IκB-α/NF-κB signaling pathway may be involved in the amelioration of QPro and QPep in DSS-induced colitis.These results indicate the potential of quinoa protein and its hydrolysate to serve as bioactive components in functional diets for intestinal health and to significantly lower intestinal inflammation.

Lactoferrin improves symptoms of dextran sulfate sodium-induced colitis in mice through modulation of cellular senescence

The multifaceted effects of lactoferrin (LF) on the digestive and immune systems make it an attractive therapeutic option in inflammatory bowel diseases. In this study, we aimed to explore the anti-inflammatory effects of LF in colitis, particularly in relation to cellular senescence. We hypothesize that LF has the potential to modulate the senescence process. The effects of LF on senescence were tested in vitro using HCT116 and SW480 cell lines, and in vivo, the dextran sulfate sodium–induced mouse model of colitis. LF (500 mg/kg) alleviated symptoms of colitis in mice with a significant decrease in colon damage (P < .0001 vs. control) and microscopic (P < .05 vs. control) scores. Cellular senescence markers p16 and p21 were significantly upregulated in the mouse colon during inflammation (both P < .01 vs. control), and LF at 500 mg/kg decreased these markers (both P < .05 vs. dextran sulfate sodium–treated mice). In vitro, LF significantly affected the expression of p16 and p21 (P < .05–P < .0001 vs. control), senescence associated secretory phenotype (P < .01–P < .0001 vs. control), and telomere-specific proteins: telomeric repeat binding factor 1 and 2 (P < .05–P < .0001 vs. control) in a concentration-dependent manner. LF modulates the expression of cellular senescence markers and shows hallmarks of senolytic and pro-senescent activity, depending on dose. Further studies are needed to fully understand the anti-inflammatory effect of LF in the context of senescence and safe utilization in patients with inflammatory bowel diseases.

Anti-inflammatory activity of peiminine in acetic acid-induced ulcerative colitis model.

Ulcerative colitis is a chronic inflammatory disorder of the intestinal mucosa and a prevalent gastrointestinal condition in developed countries. Peiminine, derived from the Fritillaria imperialis plant, exhibits remarkable anti-inflammatory and anti-cancer properties. This study aims to investigate the anti-inflammatory effects of peiminine in an experimental model of ulcerative colitis. Ulcerative colitis was induced intra-rectally in all groups, except the negative control, using 100 μl of 4% acetic acid. Peiminine treatment was initiated after ulcerative colitis induction and symptom manifestation. After the final injection, mice were sacrificed on day 15 for assessment. Various parameters were evaluated, including disease activity index, myeloperoxidase activity, nitric oxide levels, production and expression of IL-1, IL-6, TNF-α cytokines, and expression of IL-1β, IL-6, TNF-α, iNOS, and COX2 genes. Microscopic pathological evaluation was performed on colon tissue. Peiminine treatment resulted in reduced levels of NO, MPO, IL-1β, IL-6, and TNF-α. Furthermore, the expression of IL-1β, IL-6, TNF-α genes, iNOS, and COX2 genes was decreased in response to peiminine treatment in these mice. This study demonstrates the effectiveness of peiminine in alleviating inflammatory manifestations and mitigating intestinal tissue damage in an experimental model of ulcerative colitis, probably by anti-inflammatory procedure. Peiminine holds potential as a therapeutic adjunct for the management of ulcerative colitis.

Silkworm pupa protein peptide improved DSS-induced colitis in C57BL/6 mice through the MAPK/NF-κB signaling pathway

Numerous studies have revealed the multifunctional activities of silkworm pupa peptides (SPP). In this study, we investigated the protective effects of SPP on dextran sulfate sodium (DSS)-induced colitis in mice. The results showed that SPP improved the clinical symptoms of colitis in mice, including increased colon length, slowed weight loss, and reduced disease activity index (DAI) scores. Furthermore, SPP significantly alleviated DSS-induced colonic injury by reducing the expression of myeloperoxidase (MPO) in colonic tissues, enhancing mucin secretion in the colon, and decreasing colonic cell apoptosis. SPP also mitigated the severity of colitis by modulating serum inflammatory factors and improving colonic oxidative stress levels. Western blot analysis revealed that SPP suppressed the activation of the MAPK and NF-κB signaling pathways. In conclusion, SPP protected against DSS-induced colitis in mice by reducing cell apoptosis, attenuating inflammatory responses, and improving oxidative stress levels, potentially through the inhibition of MAPK and NF-κB signaling pathways.

Bergamot polysaccharides relieve DSS-induced ulcerative colitis via regulating the gut microbiota and metabolites

This study aimed to explore the efficacy of polysaccharides from bergamot (BP) in alleviating DSS-induced colitis. Results showed that BP was primarily composed of two components, BP-1 and BP-2, with similar monosaccharide compositions to BP (mainly glucose and xylose) and molecular weights (Mw) of 4.50 × 105 and 2.35 × 105 Da. This study found BP relieved disease symptoms such as weight loss and colon shortening in mice with colitis. Gut microbiota and metabolomics analysis revealed that the BP could also promote the proliferation of beneficial bacteria such as Bifidobacteria, Butyrivibrio, and Blautia, resulting in increased levels of SCFAs and L-phenylalanine, which were associated with phenylalanine, tyrosine, and tryptophan metabolism pathways. Further analysis validated the inflammatory activity of L-phenylalanine. Hence, BP may relieve colitis symptoms by regulating the gut microbiota and metabolism, which reduced inflammation and enhanced the expression of tight junctional proteins (TJ proteins) and mucin in the intestine.

Ulcerative Colitis and Nursing

Ulcerative colitis is a chronic disease of attacks and remissions characterized by bloody diarrhea, abdominal pain, and abdominal cramps involving the colonic mucosa starting from the rectum. The etiology and pathogenesis of ulcerative colitis are unknown. The most common signs and symptoms of ulcerative colitis are bloody diarrhea, abdominal pain, and abdominal cramps. Nurses, who are health professionals, are obligated to take the symptoms and signs under control and to care for patients through the treatment planned by the physician. Patient care is very important in the nursing profession. The nurse's primary role is to support the patient and his/her family to live a long, trouble-free life and comply with the treatment. This study aims to give information about Ulcerative Colitis and to discuss the nursing approach to providing professional health care.

Systematic review with meta-analysis: Diagnostic performance of faecal calprotectin in distinguishing inflammatory bowel disease from irritable bowel syndrome in adults.

Symptoms of inflammatory bowel disease (IBD) often overlap with those of irritable bowel syndrome (IBS). To evaluate the diagnostic performance of faecal calprotectin in distinguishing patients with IBD from those with IBS METHODS: We searched MEDLINE, Embase, Scopus, and Cochrane Library databases up to 1 January 2023. Studies were included if they assessed the diagnostic performance of faecal calprotectin in distinguishing IBD from IBS (defined according to the Rome criteria) using colonoscopy with histology or radiology as reference standard in adults. We calculated summary sensitivity and specificity and their 95% confidence intervals (CI) using a random-effect bivariate model. The risk of bias was assessed using the Quality Assessment of Diagnostic Accuracy Studies II. We included 17 studies with a total of 1956 patients. The summary sensitivity was 85.8% (95% CI: 78.3-91), and the specificity was 91.7% (95% CI: 84.5-95.7). At a prevalence of IBD of 1%, the negative predictive value was 99.8%, while the positive predictive value was only 9%. Subgroup analyses showed a higher sensitivity in Western than in Eastern countries (88% vs 73%) and at a cut-off of ≤50 μg/g than at >50 μg/g (87% vs. 79%), with similar estimates of specificity. All studies were at "high" or "unclear" risk of bias. Faecal calprotectin is a reliable test in distinguishing patients with IBD from those with IBS. Faecal calprotectin seems to have a better sensitivity in Western countries and at a cut-off of ≤50 μg/g.