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中药调控NLRP3炎性小体治疗急性胰腺炎的研究现状综述

An overview of current research on the modulation of NLRP3 inflammasome by traditional Chinese medicine to combat acute pancreatitis.

作者信息

He Xiongjie, Xia Jia, Chen Qi, Huang Zhaozhao, Lu Juanjuan, Ren Yisong

机构信息

Department of Critical Care Medicine, Chengdu Pidu District Hospital of Traditional Chinese Medicine, Chengdu, Sichuan, China.

Department of Endocrinology, Chengdu Pidu District Hospital of Traditional Chinese Medicine, Chengdu, Sichuan, China.

出版信息

Front Mol Biosci. 2025 Jul 16;12:1634132. doi: 10.3389/fmolb.2025.1634132. eCollection 2025.

DOI:10.3389/fmolb.2025.1634132
PMID:40740190
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12307185/
Abstract

Acute pancreatitis (AP), a life-threatening gastrointestinal emergency, is characterized by acute onset, rapid clinical deterioration, and high mortality rates, imposing profound long-term health burdens and socioeconomic costs on patients and healthcare systems. Current therapeutic strategies focus on supportive care, as no curative therapies exist to halt AP progression. Traditional Chinese medicine (TCM), with its multi-target, multi-component, and multi-pathway pharmacological properties, has emerged as a promising therapeutic drug against inflammation-driven pathologies, including AP. This review systematically discussed the assembly, activation, and pathogenic contributions of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in AP pathogenesis. Mechanistically, NLRP3 activation exacerbated pancreatic injury through caspase-1-dependent maturation of interleukin-1β (IL-1β) and gasdermin D (GSDMD)-mediated pyroptosis, perpetuating systemic inflammation. We systematically summarized the research progress of TCM in the treatment of AP by reducing pancreatic necrosis, neutrophil infiltration, and intestinal barrier dysfunction through targeting NLRP3 inflammasome, as well as its clinical evidence. Collectively, this review highlights the translational potential of TCM as an adjunctive therapy for AP through NLRP3 inflammasome inhibition, offering mechanistic insights and evidence-based support for its integration into integrative medicine strategies.

摘要

急性胰腺炎(AP)是一种危及生命的胃肠道急症,其特点是起病急、临床病情迅速恶化且死亡率高,给患者和医疗系统带来了沉重的长期健康负担和社会经济成本。目前的治疗策略侧重于支持性治疗,因为尚无治愈性疗法能够阻止AP的进展。中药具有多靶点、多成分和多途径的药理特性,已成为一种有前景的治疗药物,可用于对抗包括AP在内的炎症驱动性疾病。本综述系统地讨论了含NOD样受体家族吡咯结构域3(NLRP3)炎性小体在AP发病机制中的组装、激活及致病作用。从机制上讲,NLRP3激活通过半胱天冬酶-1依赖性的白细胞介素-1β(IL-1β)成熟和gasdermin D(GSDMD)介导的细胞焦亡加剧胰腺损伤,使全身炎症持续存在。我们系统地总结了中药通过靶向NLRP3炎性小体减少胰腺坏死、中性粒细胞浸润和肠道屏障功能障碍来治疗AP的研究进展及其临床证据。总的来说,本综述强调了中药通过抑制NLRP3炎性小体作为AP辅助治疗的转化潜力,为其纳入中西医结合策略提供了机制见解和循证支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/623e/12307185/27ceabb94c41/fmolb-12-1634132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/623e/12307185/e522c4fdb6b0/FMOLB_fmolb-2025-1634132_wc_abs.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/623e/12307185/27ceabb94c41/fmolb-12-1634132-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/623e/12307185/e522c4fdb6b0/FMOLB_fmolb-2025-1634132_wc_abs.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/623e/12307185/27ceabb94c41/fmolb-12-1634132-g001.jpg

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本文引用的文献

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Baicalein Reduces Pyroptosis of Acinar Cells in Hyperlipidemic Acute Pancreatitis by Inhibiting M1 Polarization of Macrophages via the HMGB1/TLR4/NLRP3 Pathway.黄芩素通过HMGB1/TLR4/NLRP3途径抑制巨噬细胞M1极化,减轻高脂血症性急性胰腺炎中腺泡细胞的焦亡。
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