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中华普通外科学文献(电子版) ›› 2024, Vol. 18 ›› Issue (04) : 300 -304. doi: 10.3877/cma.j.issn.1674-0793.2024.04.013

综述

NLRP3炎性小体在急性胰腺炎中作用的研究进展
李嘉兴1, 孙乙文1, 李文星1,()   
  1. 1. 030001 太原,山西医科大学第二医院普通外科
  • 收稿日期:2023-11-10 出版日期:2024-08-01
  • 通信作者: 李文星
  • 基金资助:
    山西省自然科学研究面上项目(20210302123261)

Advances in the role of NLRP3 inflammasome in acute pancreatitis

Jiaxing Li1, Yiwen Sun1, Wenxing Li1,()   

  1. 1. Department of General Surgery, the Second Hospital of Shanxi Medical University, Taiyuan 030001, China
  • Received:2023-11-10 Published:2024-08-01
  • Corresponding author: Wenxing Li
引用本文:

李嘉兴, 孙乙文, 李文星. NLRP3炎性小体在急性胰腺炎中作用的研究进展[J]. 中华普通外科学文献(电子版), 2024, 18(04): 300-304.

Jiaxing Li, Yiwen Sun, Wenxing Li. Advances in the role of NLRP3 inflammasome in acute pancreatitis[J]. Chinese Archives of General Surgery(Electronic Edition), 2024, 18(04): 300-304.

急性胰腺炎是一种与炎性反应密切相关的消化系统疾病。NOD样受体蛋白3 (NLRP3)炎性小体是一种蛋白质复合物,在炎症风暴发生、炎性状态的调节中起着至关重要的作用,其通过激活氧化应激、调节肠道菌群和驱动细胞焦亡等,影响急性胰腺炎的发生、发展和结局转归,有望成为急性胰腺炎诊断的生物标志物及治疗新靶点。现就NLRP3炎性小体与急性胰腺炎的关系以及其相互影响机制的研究现状作一综述。

Acute pancreatitis (AP) is a gastrointestinal disease closely associated with inflammatory response. The NLRP3 inflammasome is a protein complex, which plays a crucial role in the development of inflammatory storms and the regulation of inflammatory states. NLRP3 inflammasome affects the occurrence, development and outcome of AP by activating oxidative stress, regulating intestinal flora and driving cellular pyroptosis, and it is expected to become a biomarker and therapeutic target for the diagnosis of AP. The current state of research on the relationship between NLRP3 inflammasome and AP and the mechanism of their interaction are summarized.

图1 NLRP3炎性小体的经典途径、非经典途径和替代途径 NLRP3包含三个主要结构:中心核苷酸结合域、富含亮氨酸重复序列和Pyrin结构域。经典途径(左)是由TLRs受体识别PAMPs/DAMPs(包括LSP、ATP、微生物毒素、细菌表面组分和活性氧等),介导NF-κB相关信号通路,激活NLRP3炎性小体。非经典途径(中)是由革兰阴性菌的LPS启动,被小鼠的caspase-11或人的caspase-4/5识别,裂解GSDMD,激活NLRP3炎性小体。替代途径(右)仅存在于人单核细胞中,LPS被TLR4识别,通过caspase-8/FADD/RIPK3信号通路激活NLRP3炎性小体。NLRP3炎性小体通过裁剪pro-IL-1和pro-IL-18,或启动焦亡促进IL-1、IL-18释放,使细胞外IL-1、IL-18表达上调。LPS:脂多糖;PAMPs/DAMPs:病原体相关分子模式或危险相关分子模式;TLRs:Toll样受体;TLR4:Toll样受体4;ASC:凋亡相关斑点样蛋白
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