炎症小体与非酒精性脂肪性肝炎

doi:10.3969/j.issn.1672-5069.2017.03.036

摘要/Abstract

摘要： 非酒精性脂肪性肝炎（nonalcoholic steatohepatitis,NASH）的发病机制除了“二次打击”学说外,还涉及多种炎症小体及其下游信号通路的参与。炎症小体为多蛋白复合体,作为模式识别受体,识别内源性及外源性危险信号,诱发炎症级联反应,加剧肝脏损伤。核苷酸结合寡聚化结构域样受体 3（NALP3）炎症小体、NALP6炎症小体和黑色素瘤缺乏因子2（AIM2）炎症小体信号通路与NASH发生关系密切。

关键词: 非酒精性脂肪性肝炎, 核苷酸结合寡聚化结构域样受体 3, 核苷酸结合寡聚化结构域样受体 6, 黑色素瘤缺乏因子2

Abstract: Nonalcoholic steatohepatitis（NASH） is one of the most common cause of chronic liver disease worldwide. The pathogenesis of NASH includes inflammasomes signal pathway at the base of two-hit theory. The inflammasomes are multiprotein complexes that can sense danger signals from damaged cells and stimulate inflammatory cascade,thereby aggravating liver damage. In this review,we discuss the roles of neutrophilic alkaline phosphatase（NALP3）,NALP6 and absent in melanoma 2 （AIM2） inflammasome signal pathway in the pathogenesis of NASH.

Key words: Nonalcoholic steatohepatitis, Neutrophilic alkaline phosphatase 3, Neutrophilic alkaline phosphatase 6, Absent in melanoma 2

贾艳红, 李相迁, 赵彩彦. 炎症小体与非酒精性脂肪性肝炎[J]. 实用肝脏病杂志, 2017, 20(3): 377-380.

Jia Yanhong, Li Xiangqian, Zhao Caiyan. Inflammasome in the pathogenesis of nonalcoholic steatohepatitis[J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2017, 20(3): 377-380.

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