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NLRP3-细胞焦亡在实验性脓毒症肺损伤中的作用

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NOD样受体热蛋白结构域相关蛋白 3(NLRP3)介导的肺实质细胞与免疫细胞焦亡在脓毒症肺损伤的发生机制中发挥关键作用。NF-κB、JAK2/STAT3 和MAPK信号通路参与了NLRP3 介导的细胞焦亡。靶向NLRP3-细胞焦亡及其相关信号通路,Physalin B、五味子素、促红细胞生成素等药物干预,针刺足三里、肺俞穴等物理疗法,以及麦角内酯等NLRP3 特异性抑制剂,均发挥了良好的抗脓毒症肺损伤作用。本文综述NLRP3-细胞焦亡在实验性脓毒症肺损伤中的作用与机制,以及靶向NLRP3-细胞焦亡防治脓毒症肺损伤的实验研究进展,期望以NLRP3-细胞焦亡为切入点,为形成脓毒症肺损伤的防治新策略提供思考。
Role of NLRP3-pyroptosis in experimental sepsis-induced lung injury
The Nod-like receptor pyrin domain-associated protein 3(NLRP3)-mediated pyroptosis of pulmonary parenchymal and immune cells plays a key role in the pathogenesis of lung injury during sepsis.NF-κB,JAK2/STAT3 and MAPK signaling pathways are involved in NLRP3-mediated pyroptosis.Targeting NLRP3-pyroptosis and its related signaling pathways,pharmacological interventions with Physalin B,schisandrin,erythropoietin,and physical therapies such as acupuncture at Zusanli and Feishu points,as well as NLRP3-specific inhibitors like ergolide,have all shown effective anti-septic effects in treating lung injuries.This article reviewed the roles and mechanisms of NLRP3-pyroptosis in sepsis-induced lung injury,as well as the experimental progresses made in targeting NLRP3 pyroptosis as a therapy.We aim to highlight the importance of NLRP3-pyroptosis as a target,providing insights for the prevention and treatment of sepsis-induced lung injury.

Nod-like receptor pyrin domain-associated protein 3pyroptosissepsislung injury

李玉婷、牛春雨、赵自刚

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河北北方学院基础医学院&微循环研究所,张家口 075000

河北省急危重症发病机制及干预重点实验室,张家口 075000

NLRP3 细胞焦亡 脓毒症 肺损伤

国家自然科学基金

82270524

2024

中国比较医学杂志
中国实验动物学会,中国医学科学院医学实验动物研究所

中国比较医学杂志

CSTPCD北大核心
影响因子:0.473
ISSN:1671-7856
年,卷(期):2024.34(8)