Xuebijing alleviates LPS-induced acute lung injury by downregulating pro-inflammatory cytokine production and inhibiting gasdermin-E-mediated pyroptosis of alveolar epithelial cells.
10.1016/S1875-5364(23)60463-7
- Author:
Cuiping ZHANG
1
;
Xiaoyan CHEN
1
;
Tianchang WEI
1
;
Juan SONG
1
;
Xinjun TANG
1
;
Jing BI
1
;
Cuicui CHEN
1
;
Jian ZHOU
1
;
Xiao SU
2
;
Yuanlin SONG
3
,
4
,
5
,
6
,
7
Author Information
1. Shanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
2. The Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai 200031, China. Electronic address: xsu@ips.ac.cn.
3. Shanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China
4. Shanghai Institute of Infectious Disease and Biosecurity, Shanghai 200032, China
5. Shanghai Respiratory Research Institute, Shanghai 200032, China
6. National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai 200032, China
7. Department of Pulmonary Medicine, Jinshan Hospital of Fudan University, Shanghai 201508, China. Electronic address: ylsong70@163.com.
- Publication Type:Journal Article
- Keywords:
Acute lung injury;
Gasdermin-E;
Pyroptosis;
TNF-α;
Xuebijing
- MeSH:
Animals;
Mice;
Alveolar Epithelial Cells;
Pyroptosis;
Gasdermins;
Lipopolysaccharides/adverse effects*;
Tumor Necrosis Factor-alpha;
Acute Lung Injury/drug therapy*;
Respiratory Distress Syndrome
- From:
Chinese Journal of Natural Medicines (English Ed.)
2023;21(8):576-588
- CountryChina
- Language:English
-
Abstract:
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is characterized by diffuse alveolar injury primarily caused by an excessive inflammatory response. Regrettably, the lack of effective pharmacotherapy currently available contributes to the high mortality rate in patients with this condition. Xuebijing (XBJ), a traditional Chinese medicine recognized for its potent anti-inflammatory properties, exhibits promise as a potential therapeutic agent for ALI/ARDS. This study aimed to explore the preventive effects of XBJ on ALI and its underlying mechanism. To this end, we established an LPS-induced ALI model and treated ALI mice with XBJ. Our results demonstrated that pre-treatment with XBJ significantly alleviated lung inflammation and increased the survival rate of ALI mice by 37.5%. Moreover, XBJ substantially suppressed the production of TNF-α, IL-6, and IL-1β in the lung tissue. Subsequently, we performed a network pharmacology analysis and identified identified 109 potential target genes of XBJ that were mainly involved in multiple signaling pathways related to programmed cell death and anti-inflammatory responses. Furthermore, we found that XBJ exerted its inhibitory effect on gasdermin-E-mediated pyroptosis of lung cells by suppressing TNF-α production. Therefore, this study not only establishes the preventive efficacy of XBJ in ALI but also reveals its role in protecting alveolar epithelial cells against gasdermin-E-mediated pyroptosis by reducing TNF-α release.
