Protective Effect and Mechanism of Artemitin on Ozone-Induced Pulmonary Inflammation in Mice
10.12300/j.issn.1674-5817.2026.003
- VernacularTitle:艾黄素对臭氧暴露诱发小鼠肺部炎症的保护作用及机制研究
- Author:
Yanping LI
1
;
Shan HUANG
1
;
Jengyuan YAO
1
;
Yimin SHI
2
;
Huaxiu SUI
1
;
Houtan HUANG
2
;
Yanping YU
2
;
Yan MI
1
;
Tahui LIN
1
Author Information
1. Key Laboratory of Functional and Clinical Translational Medicine, Fujian Province University, Xiamen Medical College, Xiamen 361023,China
2. School of Basic Medical Sciences, Xiamen Medical College, Xiamen 361023, China
- Publication Type:Journal Article
- Keywords:
Ozone;
Artemitin;
Pulmonary inflammation;
Tumor necrosis factor-α;
Interleukin-1β;
C57BL/6 mice
- From:
Laboratory Animal and Comparative Medicine
2026;46(5):640-649
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the protective effect of artemitin against ozone (O3)-induced pulmonary inflammation in mice and to explore its underlying mechanism. MethodsThirty-two specific pathogen-free (SPF) male C57BL/6 mice were randomly divided into a blank control group, an artemitin-only control group, an O3-induced model group, and an artemitin-treated group, with 8 mice in each group. In the artemitin-treated group, animals were injected intraperitoneally with artemitin (20 mg/kg) daily, followed by a 1 h exposure to 0.000 25% O3. The artemitin-only control group received the same artemitin injection but was exposed to clean air. The O3-induced model group was injected intraperitoneally with an equal volume of normal saline daily, followed by a 1-h exposure to 0.000 25% O3. The blank control group received the saline injection and was exposed to clean air. All treatments were administered for 7 consecutive days. Pulmonary function indices of the mice in each group were measured using a whole-body plethysmography system. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (HE) staining was used to observe the histopathological changes in the lung tissue, and ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was employed for untargeted metabolomic analysis to examine the changes in overall metabolic pathways in plasma. ResultsCompared with the O3-induced model group, artemitin treatment significantly improved O3-induced lung function impairments (P<0.05), lowered the levels of TNF-α and IL-1β in BALF (P<0.05) and alleviated inflammatory cell infiltration and structural damage in lung tissues. Metabolomics results indicated that artemitin treatment compensatorily enhanced energy supply and oxidized lipid signaling, while inhibiting purine metabolism and tryptophan-derived pathways. ConclusionArtemitin exhibits a significant protective effect against O3-induced pulmonary inflammation in mice. It corrects upstream metabolic disorders by synergistically modulating tryptophan metabolism, energy metabolism, and lipid inflammatory mediators, thereby inhibiting downstream inflammatory responses and airway hyperresponsiveness. This study not only reveals the pleiotropic mechanism of artemitin in treating airway inflammation but also provides potential metabolic biomarkers and a theoretical basis for its clinical translation.
