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

被引:14
作者
Afrin, Mst. Rejina [1 ]
Arumugam, Somasundaram [1 ]
Rahman, Md. Azizur [2 ]
Karuppagounder, Vengadeshprabhu [1 ]
Sreedhar, Remya [1 ]
Harima, Meilei [1 ]
Suzuki, Hiroshi [1 ,3 ]
Nakamura, Takashi [1 ]
Miyashita, Shizuka [1 ]
Suzuki, Kenji [4 ]
Ueno, Kazuyuki [5 ]
Watanabe, Kenichi [1 ]
机构
[1] Niigata Univ Pharm & Appl Life Sci, Fac Pharmaceut Sci, Dept Clin Pharmacol, Niigata 9568603, Japan
[2] Niigata Univ, Grad Sch Med & Dent Sci, Fac Med, Dept Immunol & Med Zool, Niigata 9518510, Japan
[3] Niigata Univ, Grad Sch Med & Dent Sci, Dept Hematol Endocrinol & Metab, Niigata 9518510, Japan
[4] Niigata Univ, Grad Sch Med & Dent Sci, Dept Gastroenterol, Niigata 9518510, Japan
[5] Niigata Univ Pharm & Appl Life Sci, Dept Pharmaceut Sci, Niigata 9568603, Japan
关键词
Apoptosis; AMPK alpha; Bcl2; Colitis; Dietary supplement; IL-1; beta; Le Carbone; TNF alpha; INFLAMMATORY-BOWEL-DISEASE; NF-KAPPA-B; DEXTRAN SULFATE SODIUM; NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTOR-4; PROTEIN-KINASE; CROHNS-DISEASE; MOUSE MODEL; TNF-ALPHA; INTESTINE;
D O I
10.1016/j.intimp.2016.10.023
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 TNF alpha, IL-1 beta, p-STAT3 and p-NF-kappa B induced in the colon by DSS were markedly suppressed by LC The increased activation of AMPK alpha 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. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:70 / 78
页数:9
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