Effect and mechanism of atractyloin LPS-induced acute lung injury in mice
10.11665/j.issn.1000-5048.2025061604
- VernacularTitle:苍术素对LPS诱导的小鼠急性肺损伤的缓解作用及机制
- Author:
Meigui YOU
1
;
Hongmiao WANG
;
Yijia TANG
;
Caihua WANG
;
Yaping XU
;
Hongyuan ZHONG
Author Information
1. ;厦门医学院基础医学院, 厦门 361023厦门呼吸疾病研究所, 厦门361023;厦门医学院附属第二医院, 厦门 361023
- Publication Type:Journal Article 期刊文章
- Keywords:
atractylon;
lipopolysaccharide;
acute lung injury;
oxidative stress;
cGAS-STING pathway
- From:
Journal of China Pharmaceutical University
2025;56(6):758-765
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to investigate the anti-inflammatory and antioxidant effects of atractylon on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Changes in lung function parameters were measured in mice after intraperitoneal administration of atractylon. Pathological changes in lung tissue were observed by H&E staining, and the degree of pulmonary edema was assessed by the lung wet/dry weight ratio (W/D). Kit assays were used to detect changes in oxidative stress markers in mouse serum and the protein concentration in bronchoalveolar lavage fluid (BALF). ELISA was employed to measure the expression levels of inflammatory cytokines in BALF and serum. Western blot was used to detect the expression levels of proteins related to the cGAS-STING pathway and vascular cell adhesion molecule-1 (VCAM-1) in lung tissue. Results showed that, compared to the ALI model group, mice in the low-dose and high-dose atractylon groups exhibited significant improvement in lung function parameters, alleviated pulmonary edema, and reduced inflammatory cell infiltration in lung tissue. Protein content and inflammatory cytokine levels in serum and BALF were decreased, while serum oxidative stress indicators were improved. Western blot results further indicated that atractylon could regulate the cGAS-STING pathway, blocking the generation of inflammatory signals, and simultaneously inhibit VCAM-1 expression, thereby reducing pulmonary vascular injury. The results suggest that atractylon may alleviate LPS-induced ALI by modulating the cGAS-STING signaling pathway, reducing the expression of pro-inflammatory cytokines and the production of pro-inflammatory mediators, and improving vascular endothelial injury. This study provides a new potential target and theoretical basis for the treatment of ALI, as well as a potential drug candidate for ALI therapy.
