非经典途径IKKε和TBK1在炎症中的作用机制及药物治疗

发布时间：2018-05-11 05:59

本文选题：IKKε + TBK　；参考：《中国新药杂志》2017年13期

【摘要】：越来越多的研究发现非经典途径IKKε和TBK1在慢性炎症中起着重要作用,可促进慢性炎症细胞因子TNF-α和MCP-1等的表达,增加自身免疫性疾病和肺部炎症疾病的炎症反应,减少肥胖鼠脂肪细胞中的β-肾上腺素受体对儿茶酚胺的敏感性,降低第二信使cAMP的水平,而儿茶酚胺和cAMP均有加快能量消耗的作用。阻断IKKε和TBK1途径,可减少慢性疾病和肺部疾病的炎症反应,并减少脂肪细胞中慢性炎症因子的表达,增强胰岛素敏感性,减少胰岛素抵抗,减轻体重,起到治疗肥胖病和2型糖尿病的作用。因此,研究阻断IKKε和TBK1途径的药物治疗,对治疗慢性炎症疾病、肥胖病和2型糖尿病具有重大意义。
[Abstract]:More and more studies have found that non-classical pathways IKK 蔚 and TBK1 play an important role in chronic inflammation, promote the expression of chronic inflammatory cytokines TNF- 伪 and MCP-1, and increase the inflammatory response of autoimmune diseases and pulmonary inflammatory diseases. 尾-adrenergic receptors in adipocytes of obese rats were reduced in sensitivity to catecholamine and decreased in the level of second messenger cAMP. Both catecholamine and cAMP could accelerate energy consumption. Blocking the IKK 蔚 and TBK1 pathway can reduce the inflammatory response of chronic diseases and lung diseases, reduce the expression of chronic inflammatory factors in adipocytes, enhance insulin sensitivity, reduce insulin resistance, and reduce body weight. Play a role in the treatment of obesity and type 2 diabetes. Therefore, the study of drug therapy blocking IKK 蔚 and TBK1 pathway is of great significance in the treatment of chronic inflammatory diseases, obesity and type 2 diabetes.
【作者单位】：武汉科技大学附属天佑医院妇产科;中山大学附属第三医院肾内科;武汉科技大学附属天佑医院中心实验室;美国哈佛医学院布里格母女子医院肿瘤临床药剂科;武汉科技大学附属天佑医院肾内科;
【基金】：国家自然科学基金资助项目(81373302) 湖北省教育厅基金资助项目(530026)
【分类号】：R96

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