دورية أكاديمية

Activation of Adenosine A3 Receptor Alleviates TNF-α-Induced Inflammation through Inhibition of the NF-κB Signaling Pathway in Human Colonic Epithelial Cells

التفاصيل البيبلوغرافية
العنوان: Activation of Adenosine A3 Receptor Alleviates TNF-α-Induced Inflammation through Inhibition of the NF-κB Signaling Pathway in Human Colonic Epithelial Cells
المؤلفون: Tianhua Ren, Yumei Qiu, Weiyun Wu, Xiao Feng, Shicai Ye, Zhuang Wang, Ting Tian, Yanting He, Caiyuan Yu, Yu Zhou
المصدر: Mediators of Inflammation, Vol 2014 (2014)
بيانات النشر: Wiley, 2014.
سنة النشر: 2014
المجموعة: LCC:Pathology
مصطلحات موضوعية: Pathology, RB1-214
الوصف: To investigate the expression of adenosine A3 receptor (A3AR) in human colonic epithelial cells and the effects of A3AR activation on tumor necrosis factor alpha (TNF-α-) induced inflammation in order to determine its mechanism of action in human colonic epithelial cells, human colonic epithelial cells (HT-29 cells) were treated with different concentrations of 2-Cl-IB-MECA prior to TNF-α stimulation, followed by analysis of NF-κB signaling pathway activation and downstream IL-8 and IL-1β production. A3AR mRNA and protein were expressed in HT-29 cells and not altered by changes in TNF-α or 2-Cl-IB-MECA. Pretreatment with 2-Cl-IB-MECA prior to stimulation with TNF-α attenuated NF-κB p65 nuclear translocation as p65 protein decreased in the nucleus of cells and increased in the cytoplasm, inhibited the degradation of IκB-α, and reduced phosphorylated-IκB-α level significantly, compared to TNF-α-only-treated groups. Furthermore, 2-Cl-IB-MECA significantly decreased TNF-α-stimulated IL-8 and IL-1β mRNA expression and secretion, compared to the TNF-α-only treated group. These results confirm that A3AR is expressed in human colonic epithelial cells and demonstrate that its activation has an anti-inflammatory effect, through the inhibition of NF-κB signaling pathway, which leads to inhibition of downstream IL-8 and IL-1β expression. Therefore, A3AR activation may be a potential treatment for gut inflammatory diseases such as inflammatory bowel disease.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 0962-9351
1466-1861
Relation: https://doaj.org/toc/0962-9351; https://doaj.org/toc/1466-1861
DOI: 10.1155/2014/818251
URL الوصول: https://doaj.org/article/6233842b2af243fa8df7dc38446585fe
رقم الأكسشن: edsdoj.6233842b2af243fa8df7dc38446585fe
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:09629351
14661861
DOI:10.1155/2014/818251