ArticleJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban2013
Impact of probiotics on toll-like receptor 4 expression in an experimental model of ulcerative colitis.
Article in Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07607548 (A 8-week, Randomized, Double-blind, and Placebo-controlled Study Evaluating the Effect of Probiotic Supplementation on Proinflammatory Mechanisms Induced by Systemic Treatment in Women With Breast Cancer), which is not on this map. Cited by 7 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A 8-week, Randomized, Double-blind, and Placebo-controlled Study Evaluating the Effect of Probiotic Supplementation on Proinflammatory Mechanisms Induced by Systemic Treatment in Women With Breast Cancer
Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Effects of three different probiotics of Tibetan sheep origin and their complex probiotics on intestinal damage, immunity, and immune signaling pathways of mice infected withFrontiers in microbiology · 2023Article
- Animal Models and Pathogenesis of Ulcerative Colitis.Computational and mathematical methods in medicine · 2022Article
- Melatonin ameliorates TNBS-induced colitis in rats through the melatonin receptors: involvement of TLR4/MyD88/NF-κB signalling pathway.Inflammopharmacology · 2019Article
- Moxibustion treatment modulates the gut microbiota and immune function in a dextran sulphate sodium-induced colitis rat model.World journal of gastroenterology · 2018Article
- Evidence of the Anti-Inflammatory Effects of Probiotics and Synbiotics in Intestinal Chronic Diseases.Nutrients · 2017Review
- Effects of probiotics on Toll‑like receptor expression in ulcerative colitis rats induced by 2,4,6‑trinitro‑benzene sulfonic acid.Molecular medicine reports · 2017Article
- Preclinical Immunomodulation by the Probiotic Bifidobacterium breve M-16V in Early Life.PloS one · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are key components of the innate immune system which trigger antimicrobial host defense responses. This study aimed to investigate the impact of probiotics (Lactobacillus, Bifidobacterium) on the expression of TLR4 and tumor necrosis factor-alpha (TNF-α) in the colon mucosa of rat experimental ulcerative colitis model induced by trinitrobenzene sulfonic acid (TNBS)/ethanol and immune complexes. The gross and histological changes of the colonic mucosa were observed and assessed by the means-standard deviation and independent samples t-test. The protein expression levels of TLR4 and TNF-α were detected by using immunohistochemistry and Western blotting, respectively. It was revealed that there was visible infiltration of inflammatory cells, formation of crypt abscess, and the reduction of goblet cells in the colon tissue of experimental models. As compared with the control group, the levels of TLR4 and TNF-α protein were significantly increased in the model group (P<0.01 for both). No significant difference was found in the expression of TLR4 and TNF-α between the two-week probiotics treatment group and the model group (P>0.05), whereas significant reductions were shown in rats which were treated with probiotics for four weeks as compared with the model group (P<0.01). There was no significant difference between two probiotics-treated groups. Our results implied that probiotics were likely to play a key role in protecting ulcerative colitis by reducing the inflammatory factor TNF-α expression through inhibiting the TLR4 expression in the colon tissue of experimental models.
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