کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5555367 1559747 2017 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Le Carbone, a charcoal supplement, modulates DSS-induced acute colitis in mice through activation of AMPKα and downregulation of STAT3 and caspase 3 dependent apoptotic pathways
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Le Carbone, a charcoal supplement, modulates DSS-induced acute colitis in mice through activation of AMPKα and downregulation of STAT3 and caspase 3 dependent apoptotic pathways
چکیده انگلیسی


- Le Carbone ameliorated the severity of DSS induced colitis in mice.
- Le Carbone increased the AMPKα activation in colon.
- Le Carbone reduced the inflammatory mediators, TNFα, STAT3 and NF-κB in colitis.
- Le Carbone also activated the anti-apoptotic proteins, Bcl2 and Bcl-xL, in colon.

Le Carbone (LC) is a charcoal supplement, which contains a large amount of dietary fibers. Several studies suggested that charcoal supplement may be beneficial for stomach disorders, diarrhea, gas and indigestion. But no studies address whether LC intake would suppress inflammation, cell proliferation or disease progression in colitis. In the present study, the effect of LC on experimental colitis induced by dextran sulfate sodium (DSS) in mice and its possible mechanism of action were examined. A study was designed for 8 days, using C57BL/6 female mice that were administered with 3% DSS in drinking water for 7 days followed by another 1 day consumption of normal water with or without treatment. LC suspension was administered daily for 7 days via oral gavage using 5 mg/mouse in treatment group and normal group was supplied with drinking water. LC suspension significantly attenuated the loss of body weight and shortening of colon length induced by DSS. The disease activity index, histopathologic changes were significantly reduced by LC treatment. The inflammatory mediators TNFα, IL-1β, p-STAT3 and p-NF-κB induced in the colon by DSS were markedly suppressed by LC. The increased activation of AMPKα in the colon was also detected in LC group. Furthermore, the apoptotic marker protein cleaved caspase 3 was down-regulated and anti-apoptotic proteins Bcl2 and Bcl-xL were significantly up-regulated by LC treatment. Taken together, our results demonstrate the ability of LC to inhibit inflammation, apoptosis and give some evidence for its potential use as adjuvant treatment of inflammatory bowel disease.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 43, February 2017, Pages 70-78
نویسندگان
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