Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-κB/MAPK Pathway and Promoting IL-10/JAK1/STAT3-Mediated Anti-inflammatory Response
| العنوان: | Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-κB/MAPK Pathway and Promoting IL-10/JAK1/STAT3-Mediated Anti-inflammatory Response |
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| المؤلفون: | Tianyu Yu, Bing Xu, Lihong Chen, Mengfan Du, Guanghui Wang, Yaguang Li, Feiyu Shi |
| المصدر: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2019 (2019) |
| بيانات النشر: | Hindawi, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | MAPK/ERK pathway, Male, STAT3 Transcription Factor, Aging, Article Subject, Inflammation, Apoptosis, Pharmacology, medicine.disease_cause, Biochemistry, Acetic acid, chemistry.chemical_compound, Mice, medicine, Animals, lcsh:QH573-671, Colitis, Acetic Acid, lcsh:Cytology, Chemistry, NF-kappa B, Cell Biology, General Medicine, Janus Kinase 1, medicine.disease, Ulcerative colitis, Interleukin-10, Mice, Inbred C57BL, Toll-Like Receptor 4, TLR4, Colitis, Ulcerative, Saline Solution, medicine.symptom, Methane, Oxidative stress, Research Article, Signal Transduction |
| الوصف: | Ulcerative colitis (UC) is an inflammation-related disease involved in uncontrolled inflammation and oxidative stress and is characterized by high recurrence and relapse risk. As a rising star in gas medicine, methane owns the properties of anti-inflammation, antioxidation, and antiapoptosis. Based on the possible mechanism, we aimed to investigate the effect of methane on UC. Methane-rich saline (MRS) was introduced here, and UC was induced by acetic acid. All the C57BL/6 mice were allocated into groups as follows: control group, colitis model group, colitis treated with salazosulfapyridine (SASP) group, and colitis treated with MRS (1 or 10 ml/kg) groups. Tissue damage, the degree of inflammation, oxidative stress, and apoptosis were evaluated in the study, as well as the TLR4/NF-κB/MAPK and IL-10/JAK1/STAT3 signaling pathways for further exploration of the potential mechanism. The results showed that MRS (1) alleviated tissue damage caused by acetic acid, (2) controlled acetic acid-induced inflammation, (3) inhibited acetic acid-caused oxidative stress, (4) reduced colonic cell apoptosis due to acetic acid, (5) suppressed the TLR-4/NF-κB/MAPK signaling pathway, and (6) activated IL-10/JAK1/STAT3 anti-inflammatory response to improve the injury induced by acetic acid. We conclude that MRS has a protective effect on acetic acid-induced ulcerative colitis in mice via blocking the TLR4/NF-κB/MAPK signaling pathway and promoting the IL-10/JAK1/STAT3-mediated anti-inflammatory response. |
| وصف الملف: | text/xhtml |
| اللغة: | English |
| تدمد: | 1942-0994 1942-0900 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0c6e95c54456671952340146f931a145Test http://europepmc.org/articles/PMC6512011Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....0c6e95c54456671952340146f931a145 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19420994 19420900 |
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