ArticleWorld journal of gastroenterology2014
2,4,6-trinitrobenzene sulfonic acid-induced chronic colitis with fibrosis and modulation of TGF-β1 signaling.
Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 26 citations in OpenAlex.
- Therapeutic potential of alpha-lipoic acid on mitochondrial dynamics, oxidative/nitrosative stress, and histopathological changes in rat ulcerative colitis model.Inflammopharmacology · 2025Article
- Protective and therapeutic potentials of Trichinella spiralis larval antigen in murine induced colitis.Scientific reports · 2025Article
- Intestinal fibrosis associated with inflammatory bowel disease: Known and unknown.Chinese medical journal · 2025Review
- The Role of Claudins in the Pathogenesis of Dextran Sulfate Sodium-Induced Experimental Colitis: The Effects of Nobiletin.Biomolecules · 2024Article
- Aged garlic therapeutic intervention targeting inflammatory pathways in pathogenesis of bowel disorders.Heliyon · 2024Article
- Authors' Reply.The American journal of pathology · 2024Article
- Rectal roflumilast improves trinitrobenzenesulfonic acid-induced chronic colitis in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Article
- HIF-Overexpression and Pro-Inflammatory Priming in Human Mesenchymal Stromal Cells Improves the Healing Properties of Extracellular Vesicles in Experimental Crohn's Disease.International journal of molecular sciences · 2021Article
- Dietary salt exacerbates intestinal fibrosis in chronic TNBS colitis via fibroblasts activation.Scientific reports · 2021Article
- Sishen Pill Maintained Colonic Mucosal Barrier Integrity to Treat Ulcerative Colitis via Rho/ROCK Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Nano-Derived Therapeutic Formulations with Curcumin in Inflammation-Related Diseases.Oxidative medicine and cellular longevity · 2021Review
- Review
- The Effectiveness of Probiotics in the Treatment of Inflammatory Bowel Disease (IBD)-A Critical Review.Nutrients · 2020Review
- Herbs-Partitioned Moxibustion Combined with Acupuncture Inhibits TGF-Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Article
- Assessment of Inflammation in an Acute on Chronic Model of Inflammatory Bowel Disease with Ultrasound Molecular Imaging.Theranostics · 2015Article
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10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate whether targeting proteasome might reverse intestinal fibrosis in rats.
methodsChronic colitis was induced in rats by repeated administration of increasing dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS, 15, 30, 45, 60, 60, 60 mg) by rectal injection for 6 wk (from day 0 to day 35), while control rats received the vehicle. TNBS + bortezomib (BTZ) rats received intraperitoneal injections of BTZ twice weekly (from day 37 to day 44) at a dose of 25 mg/kg, whereas the control and TNBS groups received the same amount of the vehicle. Histologic scoring of inflammation and fibrosis was performed. Colonic production of transforming growth factor (TGF)-β was measured by ELISA. Colon fibrosis-related proteins such as phospho-p38, phospho-SMAD2/3, Akt and peroxisome proliferator activated receptor γ (PPARγ) were studied by western blot. Expression of the tight junction proteins, occludin and claudin-1, were assessed by Western blot. Colon proteasome activities (chymotrypsin-like and trypsin-like activities) were assessed.
resultsTNBS-treated rats had a higher colon weight/length ratio compared to control rats (P < 0.01). Furthermore, fibrosis and inflammation scores were higher in TNBS-treated rats compared to control rats (P < 0.01 for both). Colonic production of TGF-β production tended to be higher in TNBS-treated rats (P < 0.06). Fibrosis-related proteins such as phospho-p38, phospho-SMAD2/3, and PPARγ were significantly higher in TNBS-treated rats compared to control rats (all P < 0.05). TNBS rats had a higher expression of Akt compared to control rats (P < 0.01). Tight junction proteins were modified by repeated TNBS challenge: colon occludin expression rose significantly (P < 0.01), whereas claudin-1 expression fell (P < 0.01). Bortezomib inhibition significantly decreased chymotrypsin-like activity (P < 0.05), but had no significant effect on trypsin-like activity (P > 0.05). In contrast, bortezomib had no effect on other studied parameters such as fibrosis score, TGF-β signaling, or tight junction expression (P > 0.05 for all).
conclusionRats with TNBS-induced chronic colitis exhibited colon fibrosis associated with higher TGF-β signaling. Proteasome inhibition by bortezomib had no effect on fibrosis in our experimental conditions.
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