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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

Wang, Guanghui ; Xu, Bing ; Shi, Feiyu ; Du, Mengfan ; Li, Yaguang ; Yu, Tianyu ; Chen, Lihong Baldo, Marcelo P. ; Marcelo P Baldo

Oxidative medicine and cellular longevity, 2019-01, Vol.2019, p.7850324-12 [Periódico revisado por pares]

United States: Hindawi

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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
Autor: Wang, Guanghui ; Xu, Bing ; Shi, Feiyu ; Du, Mengfan ; Li, Yaguang ; Yu, Tianyu ; Chen, Lihong
Baldo, Marcelo P. ; Marcelo P Baldo
Assuntos: Acetic Acid - pharmacology ; Animals ; Apoptosis - drug effects ; Colitis, Ulcerative - chemically induced ; Colon ; Cytokines ; Diabetic retinopathy ; Drug dosages ; Inflammation ; Inflammatory bowel disease ; Interleukin-10 - metabolism ; Janus Kinase 1 - metabolism ; Kinases ; Male ; Medical research ; Methane - chemistry ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; Oxidative stress ; Researchers ; Saline Solution - chemistry ; Saline Solution - therapeutic use ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism ; Toll-Like Receptor 4 - metabolism ; Tumor necrosis factor-TNF
É parte de: Oxidative medicine and cellular longevity, 2019-01, Vol.2019, p.7850324-12
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Guest Editor: Marcelo P. Baldo
Descrição: 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.
Editor: United States: Hindawi
Idioma: Inglês

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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

Wang, Guanghui ; Xu, Bing ; Shi, Feiyu ; Du, Mengfan ; Li, Yaguang ; Yu, Tianyu ; Chen, Lihong Baldo, Marcelo P. ; Marcelo P Baldo

United States: Hindawi

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