کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8437438 | 1546869 | 2018 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sodium Butyrate Inhibits Inflammation and Maintains Epithelium Barrier Integrity in a TNBS-induced Inflammatory Bowel Disease Mice Model
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کلمات کلیدی
GPR109AMuc2LPSTNBSFITCDSSCLDN1PBSIBD2,4,6-Trinitrobenzene sulfonic acid - 2،4،6-ترینیتروبنسل سولفونیک اسیدinflammation - التهاب( توروم) Inflammatory bowel disease - بیماریهای التهابی رودهSodium butyrate - سدیم butyrateDextran sulfate sodium - سولفات سدیم دکسترانPhosphate buffered saline - فسفات بافر شورfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتlipopolysaccharide - لیپوپلی ساکاریدmucin-2 - موین-2wild-type - نوع وحشیClaudin-1 - کلودین-1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
G Protein Coupled Receptor 109A (GPR109A), which belongs to the G protein coupled receptor family, can be activated by niacin, butyrate, and β-hydroxybutyric acid. Here, we assessed the anti-inflammatory activity of sodium butyrate (SB) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis mice, an experimental model that resembles Crohn's disease, and explored the potential mechanism of SB in inflammatory bowel disease (IBD). In vivo, experimental GPR109aâ/â and wild-type (WT) mice were administered SB (5 g/L) in their drinking water for 6 weeks. The mice were then administered TNBS via rectal perfusion to imitate colitis. In vitro, RAW246.7 macrophages, Caco-2 cells, and primary peritoneal macrophages were used to investigate the protective roles of SB on lipopolysaccharide (LPS)-induced inflammatory response and epithelium barrier dysfunction. In vivo, SB significantly ameliorated the inflammatory response and intestinal epithelium barrier dysfunction in TNBS-induced WT mice, but failed to provide a protective effect in TNBS-induced GPR109aâ/â mice. In vitro, pre-treatment with SB dramatically inhibited the expression of TNF-α and IL-6 in LPS-induced RAW246.7 macrophages. SB inhibited the LPS-induced phosphorylation of the NF-κB p65 and AKT signaling pathways, but failed to inhibit the phosphorylation of the MAPK signaling pathway. Our data indicated that SB ameliorated the TNBS-induced inflammatory response and intestinal epithelium barrier dysfunction through activating GPR109A and inhibiting the AKT and NF-κB p65 signaling pathways. These findings therefore extend the understanding of GPR109A receptor function and provide a new theoretical basis for treatment of IBD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: EBioMedicine - Volume 30, April 2018, Pages 317-325
Journal: EBioMedicine - Volume 30, April 2018, Pages 317-325
نویسندگان
Guangxin Chen, Xin Ran, Bai Li, Yuhang Li, Dewei He, Bingxu Huang, Shoupeng Fu, Juxiong Liu, Wei Wang,