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首页> 外文期刊>The Journal of Nutritional Biochemistry >Suppression of intestinal inflammation and inflammation-driven colon cancer in mice by dietary sphingomyelin: importance of peroxisome proliferator-activated receptor gamma expression.
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Suppression of intestinal inflammation and inflammation-driven colon cancer in mice by dietary sphingomyelin: importance of peroxisome proliferator-activated receptor gamma expression.

机译：饮食鞘磷脂抑制小鼠肠道炎症和炎症驱动的结肠癌：过氧化物酶体增殖物激活受体γ表达的重要性。

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摘要

Inflammation of the gastrointestinal tract increases the risk of developing colon cancer especially in younger adults. Dietary compounds are not only associated with the etiology of inflammation and colon cancer but also in their prevention. Sphingolipid metabolites have been shown to play a role in the initiation and perpetuation of inflammatory responses. In the present study, we investigated the suppression of dextran sodium sulfate-induced colitis and azoxymethane-induced colon cancer by dietary sphingomyelin (SM) in mice that lack functional peroxisome proliferator-activated receptor gamma (PPAR- gamma) in intestinal epithelial and immune cells. Dietary SM decreased disease activity and colonic inflammatory lesions in mice of both genotypes but more efficiently in mice expressing PPAR- gamma. The increased survival and suppression of tumor formation in the SM-fed mice appeared to be independent of PPAR- gamma expression in immune and epithelial cells. Using a real-time polymerase chain reaction array, we detected an up-regulation in genes involved in Th1 (interferon gamma) and Th17 (interleukin [IL]-17 and IL-23) responses despite the reduced inflammation scores. However, the genes involved in Th2 (IL-4, IL-13 and IL-13ra2) and Treg (IL-10rb) anti-inflammatory responses were up-regulated in a PPAR- gamma-dependent manner. In line with the PPAR- gamma dependency of our in vivo findings, treatment of RAW macrophages with sphingosine increased the PPAR- gamma reporter activity. In conclusion, dietary SM modulated inflammatory responses at the early stages of the disease by activating PPAR- gamma, but its anticarcinogenic effects followed a PPAR- gamma-independent pattern. All rights reserved, Elsevier.
机译：胃肠道发炎会增加患结肠癌的风险，尤其是在年轻人中。饮食化合物不仅与炎症和结肠癌的病因有关，而且与它们的预防有关。已经显示鞘脂代谢物在炎性反应的引发和持久中起作用。在本研究中，我们研究了饮食鞘磷脂（SM）对在肠道上皮细胞和免疫细胞中缺乏功能性过氧化物酶体增殖物激活受体γ（PPAR-γ）的小鼠抑制右旋糖酐硫酸钠诱导的结肠炎和乙氧基甲烷诱导的结肠癌的抑制作用。日粮SM降低两种基因型小鼠的疾病活动性和结肠炎性病变，但在表达PPAR-γ的小鼠中更有效。 SM喂养小鼠中存活率的提高和肿瘤形成的抑制似乎独立于免疫和上皮细胞中的PPAR-γ表达。使用实时聚合酶链反应阵列，尽管炎症评分降低，我们仍检测到参与Th1（干扰素γ）和Th17（白介素[IL] -17和IL-23）应答的基因上调。然而，涉及Th2（IL-4，IL-13和IL-13ra2）和Treg（IL-10rb）抗炎反应的基因以PPAR-γ依赖性方式上调。与我们体内发现的PPAR-γ依赖性相一致，用鞘氨醇治疗RAW巨噬细胞可提高PPAR-γ报道分子的活性。总之，饮食SM通过激活PPAR-γ调节疾病早期的炎症反应，但其抗癌作用遵循PPAR-γ独立模式。保留所有权利，Elsevier。

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