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首页> 外文期刊>Inflammatory bowel diseases >Inflammation and Inflammatory Cytokine Contribute to the Initiation and Development of Ulcerative Colitis and Its Associated Cancer
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Inflammation and Inflammatory Cytokine Contribute to the Initiation and Development of Ulcerative Colitis and Its Associated Cancer

机译:炎症和炎症细胞因子有助于溃疡性结肠炎的开始和发育及其相关癌症

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摘要

Dysregulated inflammatory responses play a pivotal role in the initiation, development, and progression of tumors, as demonstrated by the association between ulcerative colitis and the increased risk of colon carcinoma. In this review, the underlying mechanisms for the initiation and development of ulcerative colitis and colitis-associated cancer are described, mainly focusing on the inflammation and inflammatory cytokine. Disruption of the intestinal mucosal barrier and bacterial invasion resulted in intestinal inflammation; and further TLR4/NF-kappa B stimulation in intestinal epithelial cells, inflammatory cell infiltration, and inflammatory cytokine release all confer survival advantages to or promote abnormal proliferation in susceptible cells. Importantly, the respective roles of TLR4/NF-kappa B, TNF-alpha, and IL-6 in intestinal epithelial cells and inflammatory cells are summarized in detail. A thorough understanding of these molecular mechanisms may help researchers and clinicians to explore novel approaches for the prevention and treatment of colitis-associated cancer.
机译:具有吸引力的炎症反应在肿瘤的开始,发育和进展中起着枢轴作用,如溃疡性结肠炎之间的关联和结肠癌的风险增加所示。在本文中,描述了溃疡性结肠炎和结肠炎相关癌症启动和发展的潜在机制,主要关注炎症和炎症细胞因子。肠粘膜屏障和细菌侵袭的破坏导致肠炎;并且在肠上皮细胞,炎症细胞浸润和炎症细胞因子释放的进一步TLR4 / NF-Kappa B刺激全部赋予生存优势或促进易感细胞中的异常增殖。重要的是,详细概述了肠上皮细胞和炎性细胞中TLR4 / NF-κB,TNF-α和IL-6的各自作用。彻底了解这些分子机制可能有助于研究人员和临床医生探索结肠炎相关癌症预防和治疗的新方法。

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