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Le Carbone, a charcoal supplement, modulates DSS-induced acute colitis in mice through activation of AMPK alpha and downregulation of STAT3 and caspase 3 dependent apoptotic pathways

机译:乐货物,一种木炭补充剂,通过激活AMPKα和Dat3和Caspase 3依赖性凋亡途径的激活来调节小鼠的DSS诱导的急性结肠炎

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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.
机译:Le Carbone(LC)是一种木炭补充剂,含有大量的膳食纤维。一些研究表明木炭补充剂可能对胃部疾病,腹泻,天然气和消化不良有益。但没有研究表明LC摄入是否会抑制结肠炎的炎症,细胞增殖或疾病进展。在本研究中,研究了LC对小鼠的硫酸硫酸钠(DSS)诱导的实验性结肠炎及其可能的作用机制。设计了8天,使用C57BL / 6雌性小鼠,用3%DSS在饮用水中施用7天,然后另外1天的普通水消耗,有或没有治疗。通过使用5mg /小鼠在治疗组中使用5mg /小鼠每天每天服用LC悬浮液,并用饮用水供应正常组。 LC悬浮液显着抑制了DSS诱导的体重减轻和缩短结肠长度。通过LC处理显着降低了疾病活性指数,组织病理学变化显着降低。通过DSS在结肠中诱导的炎症介质TNFα,IL-1β,P-STAT3和P-NF-Kappa B通过LC抑制了在LC基团中检测到结肠中的AMPKα的增加的增加。此外,细胞凋亡标记蛋白切割的胱天蛋白3是下调的,通过LC处理显着上调抗凋亡蛋白Bcl2和Bcl-XL。我们的结果一起展示了LC抑制炎症,细胞凋亡的能力,并提供了潜在用途作为炎症性肠病的辅助治疗的潜在用途。 (c)2016年Elsevier B.v.保留所有权利。

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