Numerous lines of evidence support a relationship between intestinal inflammation and cancer. Therefore, much attention has recently been focused on the identification of natural compounds with anti-inflammatory activities as a strategy to suppress the early stages of colorectal cancer. Because cocoa is a rich source of bioactive compounds, the present study investigated its anti-inflammatory properties in a rat model of azoxymethane (AOM)-induced colon carcinogenesis and in TNF-α-stimulated Caco-2 cells. A total of forty male rats were fed with control or cocoa-enriched diets (12 %) during 8 weeks and injected with saline or AOM (20 mg/kg body weight) during the third and fourth week (n 10 rats/group). At the end of the experiment, colon samples were evaluated for markers of inflammation. The anti-inflammatory activity of a cocoa polyphenolic extract (10 μg/ml) was examined in TNF-α-stimulated Caco-2 cells, an in vitro model of experimentally induced intestinal inflammation. The signalling pathways involved, including NF-κB and the mitogen-activated protein kinase family such as c-Jun NH₂-terminal kinases (JNK), extracellular signal-regulated kinases and p38, were also evaluated. The results show that the cocoa-rich diet decreases the nuclear levels of NF-κB and the expression of pro-inflammatory enzymes such as cyclo-oxygenase-2 and inducible NO synthase induced by AOM in the colon. Additionally, the experiments in Caco-2 cells confirm that cocoa polyphenols effectively down-regulate the levels of inflammatory markers induced by TNF-α by inhibiting NF-κB translocation and JNK phosphorylation. We conclude that cocoa polyphenols suppress inflammation-related colon carcinogenesis and could be promising in the dietary prevention of intestinal inflammation and related cancer development.

译文

:大量证据支持肠道炎症与癌症之间的关系。因此,近来许多注意力集中在鉴定具有抗炎活性的天然化合物上,作为抑制结直肠癌早期阶段的策略。由于可可是生物活性化合物的丰富来源,因此本研究在由乙氧基甲烷(AOM)诱导的结肠癌发生的大鼠模型中以及在TNF-α刺激的Caco-2细胞中研究了其抗炎特性。总共40只雄性大鼠在8周内接受了对照或富含可可的饮食(12%),并在第三和第四周内注射了盐水或AOM(20 mg / kg体重)(每组10只大鼠)。在实验结束时,评估结肠样品的炎症标志物。在可诱导肠道炎症的体外模型TNF-α刺激的Caco-2细胞中检测了可可多酚提取物(10μg/ ml)的抗炎活性。还评估了涉及的信号通路,包括NF-κB和丝裂原活化的蛋白激酶家族,例如c-Jun NH 2末端激酶(JNK),细胞外信号调节激酶和p38。结果表明,富含可可的饮食降低了结肠中NF-κB的核水平,降低了AOM诱导的促炎性酶(如环氧化酶2和可诱导的NO合酶)的表达。此外,在Caco-2细胞中进行的实验证实,可可多酚通过抑制NF-κB易位和JNK磷酸化,有效下调TNF-α诱导的炎症标志物的水平。我们得出的结论是,可可多酚抑制炎症相关的结肠癌发生,并且在饮食预防肠道炎症和相关的癌症发展中可能很有希望。

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