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首页> 外文期刊>The Journal of Nutritional Biochemistry >Curcumin prevents leptin-induced tight junction dysfunction in intestinal Caco-2 BBe cells.
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Curcumin prevents leptin-induced tight junction dysfunction in intestinal Caco-2 BBe cells.

机译：姜黄素可预防瘦素诱导的肠道Caco-2 BBe细胞紧密连接功能障碍。

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Maintaining tight junction (TJ) integrity in the intestine is critical for nutrient absorption, host defense, and host immunity. While leptin secreted from adipose tissue is associated with obesity and obesity-related intestinal inflammation, the role of luminal leptin in intestinal TJ function is elusive. Here, we examined the role of leptin in intestinal TJ function in Caco-2 BBe cells and further explored the function of curcumin (CCM) in leptin-induced TJ dysfunction. Apical leptin, but not basolateral leptin, treatment at a concentration of 100 ng/ml deteriorated TJ function in Caco-2 BBe cells. Leptin-impaired TJ alteration was resulted from induction of leptin receptor-dependent JAK2/STAT3 signaling pathway and its-related PI3K/Akt/ERK1/2 signaling pathways. Apical leptin also lowered the expression levels of genes encoding TJ-associated proteins such as zonula occludens-3, claudin-5, and occludin, and elevated expression of pro-inflammatory genes such as IL-6 and TNF- alpha . Leptin-impaired TJ junction in Caco-2 BBe cells was blunted by a 30-min CCM pretreatment through inhibition of leptin receptor-dependent signaling pathway, and its-associated induction of expression of genes encoding TJ-associated proteins and pro-inflammatory cytokines. Our results elucidate a novel function of luminal leptin in intestinal TJ dysfunction, and further identify CCM as an effective dietary compound that prevents leptin-impaired TJ function in intestinal cells.
机译：维持肠内紧密连接（TJ）的完整性对于营养吸收，宿主防御和宿主免疫至关重要。虽然从脂肪组织分泌的瘦素与肥胖症和肥胖症相关的肠道炎症有关，但管腔瘦素在肠道TJ功能中的作用却难以捉摸。在这里，我们检查了瘦素在Caco-2 BBe细胞中肠道TJ功能中的作用，并进一步探索了姜黄素（CCM）在瘦素诱导的TJ功能障碍中的功能。以100 ng / ml的浓度处理顶基瘦素而非基底外侧瘦素会使Caco-2 BBe细胞的TJ功能恶化。瘦素受损的TJ改变是由瘦素受体依赖性JAK2 / STAT3信号通路及其相关的PI3K / Akt / ERK1 / 2信号通路的诱导引起的。顶端瘦素还降低了编码TJ相关蛋白（例如小带闭合蛋白-3，claudin-5和闭合蛋白）的基因的表达水平，并提高了促炎基因（例如IL-6和TNF-α）的表达。 Caco-2 BBe细胞中的瘦素受损TJ连接通过30分钟的CCM预处理而受到钝化，其作用是抑制瘦素受体依赖性信号传导途径，以及其与编码TJ相关蛋白和促炎细胞因子基因表达的相关诱导。我们的结果阐明了肠瘦素在肠TJ功能障碍中的新功能，并进一步确定CCM为有效的饮食化合物，可预防肠细胞中瘦素受损的TJ功能。

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