细胞焦亡在脓毒症相关肝损伤中的作用机制及干预药物的研究进展

doi:10.3877/cma.j.issn.2095-1221.2025.06.008

中华细胞与干细胞杂志(电子版) ›› 2025, Vol. 15 ›› Issue (06) : 374 -382. doi: 10.3877/cma.j.issn.2095-1221.2025.06.008

综述

细胞焦亡在脓毒症相关肝损伤中的作用机制及干预药物的研究进展

安嘉伟¹^,³, 刘国臣¹^,³, 朱俊宇¹, 盖新宇²^,^†(

)

¹400042　重庆，陆军军医大学大坪医院战伤感染与特需药品研究室，创伤与化学中毒全国重点实验室
²573100　海口，海南医科大学第二附属医院急诊科，海南省急危重症临床医学研究中心
³400038　重庆，陆军军医大学基础医学院

收稿日期:2025-08-11 出版日期:2025-12-01
通信作者: 盖新宇
基金资助:
海南省卫生健康科技创新联合项目(WSJK2025QN117，WSJK2025ZD221)

Advances in the mechanism of pyroptosis in sepsis-associated liver injury and intervention drugs

Jiawei An¹^,³, Guocheng Liu¹^,³, Junyu Zhu¹, Xinyu Gai²^,^†()

¹Department of Wound Infection and Drug, Daping Hospital, Army Medical University, State Key Laboratory of Trauma and Chemical Poisoning, Chongqing 400042, China
²Emergency Department of the Second Affiliated Hospital of Hainan Medical University, the Emergency and Critical Care Clinical Medicine Research Center of Hainan, Haikou 573100, China
³College of Basic Medicine, Army Medical University, Chongqing 400038, China

Received:2025-08-11 Published:2025-12-01
Corresponding author: Xinyu Gai

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引用本文：

安嘉伟, 刘国臣, 朱俊宇, 盖新宇. 细胞焦亡在脓毒症相关肝损伤中的作用机制及干预药物的研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2025, 15(06): 374-382.

Jiawei An, Guocheng Liu, Junyu Zhu, Xinyu Gai. Advances in the mechanism of pyroptosis in sepsis-associated liver injury and intervention drugs[J/OL]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2025, 15(06): 374-382.

脓毒症是由宿主感染反应失调引发的致命性器官功能障碍综合征，具有高发病率和高病死率的特点。肝脏是脓毒症进程中关键代谢与免疫器官，而脓毒症相关肝损伤（SALI）是脓毒症患者死亡率独立的预测指标，肝功能障碍会严重损害其预后，减轻SALI是降低脓毒症患者死亡率的关键。SALI的发病机制复杂，细胞焦亡作为促炎程序性细胞死亡形式，在其中发挥关键作用。细胞焦亡通过经典（NLRP3-caspase-1-GSDMD）及非经典（caspase-4/5/11-GSDMD）途径调控。肝脏中肝实质细胞、肝巨噬细胞和中性粒细胞等不同类型细胞的焦亡，通过炎症放大和微循环障碍等机制参与SALI进程。目前，临床上现有的部分护肝药物已被证实具有抗焦亡的作用。一些天然化合物、人工合成药物、内源性活性分子及干细胞治疗等也可通过调控焦亡通路减轻SALI。综上，细胞焦亡是SALI的关键机制，深入探究其调控机制及干预药物，可为SALI精准防治提供新策略。

关键词: 脓毒症, 肝损伤, 细胞焦亡, 药物

Sepsis is a life-threatening organ dysfunction syndrome caused by dysregulation of the host's response to infection, characterized by high morbidity and mortality. The liver is a key metabolic and immune organ in the progression of sepsis, and sepsis-associated liver injury (SALI) is an independent predictor of mortality in sepsis patients. Hepatic dysfunction can severely impair their prognosis, and alleviating SALI is crucial for reducing the mortality of sepsis patients. The pathogenesis of SALI is complex, and pyroptosis, as a pro-inflammatory form of programmed cell death, plays a key role in it. Pyroptosis is regulated through classical (NLRP3-caspase-1-GSDMD) and non-classical (caspase-4/5/11-GSDMD) pathways. The pyroptosis of different cell types in the liver, such as hepatocytes, hepatic macrophages, and neutrophils, can participate in the process of SALI through mechanisms such as inflammation amplification and microcirculatory disturbance. At present, some existing hepatoprotective drugs in clinical practice have been proven to have anti-pyroptotic effects. Some natural compounds, synthetic drugs, endogenous active molecules, and stem cell therapy can also alleviate SALI by regulating pyroptosis pathways. In conclusion, pyroptosis is a key mechanism of SALI, and in-depth exploration of its regulatory mechanisms and intervention drugs can provide new strategies for the precise prevention and treatment of SALI.

Key words: Sepsis, Liver Injury, Pyroptosis, Drug

图1 肝脏中不同细胞类型的焦亡在SALI中的作用机制

图2 不同护肝药物抗焦亡主要机制

表1 不同药物调控细胞焦亡缓解SALI的机制

药物/治疗	动物诱导模型	抗焦亡机制	损伤缓解表现	文献
黄精多糖	LPS	抑制NLRP3→阻断caspase-1/GSDMD焦亡	血清ALT/AST趋近正常；肝组织IL-1β/IL-18降低超过50%；肝组织病理改善	[51]
茶黄素	LPS	抑制NLRP3→抑制caspase-1/GSDMD-NT→阻断焦亡	血清IL-1β降低；肝组织caspase-1活性下降	[52]
甘草苷XLIX	CLP	调控NF-κB/PPAR-α→阻断NLRP3焦亡	肝组织NLRP3降低；血清ALT/AST降低	[53]
黄芪甲苷Ⅳ	LPS+D-gal	激活AMPK/SIRT1→抑制caspase-11/GSDMD→抑制焦亡	血清ALT/AST降低40%~ 60%；肝组织坏死面积减小≥50%	[54]
姜黄素	LPS	激活Nrf2/HO-1→降低ROS→抑制NLRP3/caspase-1/GSDMD焦亡	血清ALT/AST降低30%~ 50%；肝组织炎症浸润减小40%~ 50%；肝IL-1β/IL-18 mRNA降低60%+	[55]
TLR4抑制剂	腹腔注射大肠杆菌	抑制TLR4→阻断NLRP3/GSDMD焦亡	肝组织TLR4/GSDMD-N降低；血清IL-1β降低	[56]
CD38激活剂	腹腔注射大肠杆菌	激活CD38→反向调控TLR4-NLRP3→抑制焦亡	血清ALT/AST降低；小鼠存活率升高	[56]
Samotolisib	LPS	激活PI3K/AKT→升高Nedd4→降解caspase-11→抑制焦亡	肝组织caspase-11活性下降；血清ALT/AST降低	[57]
沙罗格列肽	LPS	抑制caspase-11+NLRP3→抑制经典+非经典焦亡	肝组织caspase-11/NLRP3降低；肝损伤缓解	[58]
IAA94	LPS	抑制CLICs→阻断NEK7-NLRP3→抑制NLRP3焦亡	肝脏炎症浸润减小；肝组织损伤面积减小	[59]
二甲基富马酸（DMF）	CLP	抑制caspase-11→阻断非经典焦亡	肝组织caspase-11降低；血清ALT/AST降低	[60]
雌激素	LPS	靶向NLRP3→抑制caspase-1/IL-1β→阻断焦亡	血清AST/ALT降低；肝细胞焦亡率降低	[61]
谷氨酰胺	CLP	晚期：阻断焦亡通路→维持焦亡平衡	脓毒症晚期ALT/AST降低；+抗生素→肝损伤缓解	[62]
辅酶Q10	CLP	抑制NLRP3→降低IL-1β→抑制焦亡	肝组织NLRP3/IL-1β降低；血清ALT/AST降低	[63]
鸢尾素	LPS	抑制NF-κB→降低NLRP3/caspase-1→抑制焦亡	肝组织NLRP3/GSDMD降低；血清ALT/AST降低	[64]
IRG1/衣康酸	LPS	抑制GSDMD +激活Nrf2→抑制NLRP3焦亡	血清ALT/AST降低；肝组织GSDMD-N/NLRP3降低	[65]
骨髓间充质干细（BMSC）移植	LPS	旁分泌→降低NLRP3/IL-1β→阻断肝细胞/巨噬细胞焦亡	血清IL-1β/IL-18降低；肝细胞坏死面积减小	[66]

表1 不同药物调控细胞焦亡缓解SALI的机制

药物/治疗	动物诱导模型	抗焦亡机制	损伤缓解表现	文献
黄精多糖	LPS	抑制NLRP3→阻断caspase-1/GSDMD焦亡	血清ALT/AST趋近正常；肝组织IL-1β/IL-18降低超过50%；肝组织病理改善	[51]
茶黄素	LPS	抑制NLRP3→抑制caspase-1/GSDMD-NT→阻断焦亡	血清IL-1β降低；肝组织caspase-1活性下降	[52]
甘草苷XLIX	CLP	调控NF-κB/PPAR-α→阻断NLRP3焦亡	肝组织NLRP3降低；血清ALT/AST降低	[53]
黄芪甲苷Ⅳ	LPS+D-gal	激活AMPK/SIRT1→抑制caspase-11/GSDMD→抑制焦亡	血清ALT/AST降低40%~ 60%；肝组织坏死面积减小≥50%	[54]
姜黄素	LPS	激活Nrf2/HO-1→降低ROS→抑制NLRP3/caspase-1/GSDMD焦亡	血清ALT/AST降低30%~ 50%；肝组织炎症浸润减小40%~ 50%；肝IL-1β/IL-18 mRNA降低60%+	[55]
TLR4抑制剂	腹腔注射大肠杆菌	抑制TLR4→阻断NLRP3/GSDMD焦亡	肝组织TLR4/GSDMD-N降低；血清IL-1β降低	[56]
CD38激活剂	腹腔注射大肠杆菌	激活CD38→反向调控TLR4-NLRP3→抑制焦亡	血清ALT/AST降低；小鼠存活率升高	[56]
Samotolisib	LPS	激活PI3K/AKT→升高Nedd4→降解caspase-11→抑制焦亡	肝组织caspase-11活性下降；血清ALT/AST降低	[57]
沙罗格列肽	LPS	抑制caspase-11+NLRP3→抑制经典+非经典焦亡	肝组织caspase-11/NLRP3降低；肝损伤缓解	[58]
IAA94	LPS	抑制CLICs→阻断NEK7-NLRP3→抑制NLRP3焦亡	肝脏炎症浸润减小；肝组织损伤面积减小	[59]
二甲基富马酸（DMF）	CLP	抑制caspase-11→阻断非经典焦亡	肝组织caspase-11降低；血清ALT/AST降低	[60]
雌激素	LPS	靶向NLRP3→抑制caspase-1/IL-1β→阻断焦亡	血清AST/ALT降低；肝细胞焦亡率降低	[61]
谷氨酰胺	CLP	晚期：阻断焦亡通路→维持焦亡平衡	脓毒症晚期ALT/AST降低；+抗生素→肝损伤缓解	[62]
辅酶Q10	CLP	抑制NLRP3→降低IL-1β→抑制焦亡	肝组织NLRP3/IL-1β降低；血清ALT/AST降低	[63]
鸢尾素	LPS	抑制NF-κB→降低NLRP3/caspase-1→抑制焦亡	肝组织NLRP3/GSDMD降低；血清ALT/AST降低	[64]
IRG1/衣康酸	LPS	抑制GSDMD +激活Nrf2→抑制NLRP3焦亡	血清ALT/AST降低；肝组织GSDMD-N/NLRP3降低	[65]
骨髓间充质干细（BMSC）移植	LPS	旁分泌→降低NLRP3/IL-1β→阻断肝细胞/巨噬细胞焦亡	血清IL-1β/IL-18降低；肝细胞坏死面积减小	[66]

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Advances in the mechanism of pyroptosis in sepsis-associated liver injury and intervention drugs

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Advances in the mechanism of pyroptosis in sepsis-associated liver injury and intervention drugs