霍乱毒素B亚基和肽LKEKK抑制肠上皮细胞TNF-α信号并减轻结肠炎小鼠模型的炎症

Elena V Navolotskayaa, V. B. Sadovnikov, V. Lipkin, V. Zav'yalov
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引用次数: 2

摘要

在人Caco-2肠上皮细胞中,胸腺素-α1 16-20序列和干扰素-α2 131-135序列对应的霍乱毒素B亚基(CT-B)和合成肽LKEKK(浓度范围100-5000µM)显著降低TNF-α刺激的促炎细胞因子的表达,增加抗炎细胞因子IL-10的表达。在右旋糖酐硫酸钠诱导的结肠炎CT-B和肽小鼠模型中,LKEKK (20 mg/kg体重口服14天)可降低TNF-α和IL-6的产生,并降低炎症的严重程度。因此,CT-B和肽LKEKK在体外和体内均能抑制炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cholera Toxin B Subunit and Peptide LKEKK Inhibit TNF-α Signaling in Intestinal Epithelial Cells and Reduce Inflammation in a Mouse Model of Colitis
Cholera toxin B subunit (CT-B) and synthetic peptide LKEKK corresponding to the sequence 16-20 of thymosin-α1 and the sequence 131-135 of interferon-α2 (the concentration range of 100-5000 µM) significantly reduced TNF-α-stimulated pro-inflammatory cytokine expression and increases the expression of the anti-inflammatory cytokine IL-10 in human Caco-2 intestinal epithelial cells. In a mouse model of dextran sodium sulfate-induced colitis CT-B and peptide, LKEKK (20 mg/kg body weight orally for 14 days) decreased the production of TNF-α and IL-6, as well as the severity of inflammation. Thus, CT-B and peptide LKEKK are able to suppress inflammation in vitro and in vivo.
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