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Opposite effects of sevoflurane at high and low concentration on the airway inflammation in juvenile asthma rats: A
Feng-Lin Wang1, Yan-Nan Zhou2, Guang-Ting Zhang2
1Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China; Anesthesiology & Operation Department, Suining Central Hospital, SuiNing, China.
Insights
Sevoflurane affects juvenile asthmatic rat airways differently based on concentration. High concentrations (3.2%) reduce inflammation, while low concentrations (0.4%) worsen it, highlighting key protein roles.
Area of Science:
- Anesthesiology
- Pediatric Respiratory Medicine
- Molecular Biology
Background:
- High incidence of sevoflurane-related respiratory events in asthmatic children.
- Limited understanding of sevoflurane concentration-specific effects on pediatric asthmatic airways.
Purpose of the Study:
- To investigate the impact of varying sevoflurane concentrations on juvenile asthmatic rat airways.
- To identify molecular mechanisms underlying sevoflurane's concentration-dependent effects.
Main Methods:
- Established an ovalbumin (OVA)-induced juvenile rat asthma model.
- Evaluated airway irritation, ventilation, pathology, and inflammation.
- Utilized TMT-based proteomics and bioinformatics, validated by western blot.
Main Results:
- Sevoflurane's effects were concentration-dependent: 3.2% alleviated symptoms, while 0.4% exacerbated them.
- Proteomics identified differentially expressed proteins (DEPs) involved in inflammation and immune response.
- Key proteins like MHC1, MHC2, and VAV1 showed opposing expression patterns based on sevoflurane concentration.
Conclusions:
- Sevoflurane exhibits opposing effects on asthmatic airways depending on concentration.
- MHC1, MHC2, and VAV1 are identified as critical mediators of these differential effects.
- These proteins represent potential therapeutic targets for managing sevoflurane's impact in asthmatic patients.
Background:
The incidence of sevoflurane-related adverse respiratory events in children with asthma is notably high. During different phases of sevoflurane anesthesia, asthmatic children's airways are exposed to varying concentrations of the anesthetic. However, the specific effects of different concentrations of sevoflurane on the developing airways with asthmatic hyperreactivity have not been systematically studied.
Methods:
An ovalbumin (OVA)-induced juvenile rat asthma model was established to evaluate the impact of varying sevoflurane concentrations on airway irritation symptoms, ventilation, pathological scoring, and inflammation. Tandem mass tag (TMT)-based quantitative proteomics and bioinformatics analyses were conducted, with key protein expressions validated by western blot.
Results:
Sevoflurane alleviated airway irritation symptoms in OVA-treated rats in a concentration-dependent manner. At 3.2 %, sevoflurane significantly reduced peribronchial inflammation, while 0.4 % sevoflurane exacerbated hypoxia, peribronchial injury, and inflammation. Proteomic analysis identified 54 overlapping differentially expressed proteins (DEPs), with three (serine protease inhibitor (SerpinA3L), major histocompatibility complex 1 (MHC1), and major histocompatibility complex 2 (MHC2)) being upregulated in the 3.2 % sevoflurane group but downregulated in the 0.4 % sevoflurane group. DEPs were predominantly linked to lysosomal and phagosomal pathways, as well as antigen processing and presentation. Three key hub proteins-cathepsin (CAT), vav guanine nucleotide exchange factor 1 (VAV1), and C-reactive protein (CRP)-were identified, and their expression levels were validated, matching the bioinformatics analysis results.
Conclusions:
Our findings demonstrate that sevoflurane exerts opposing effects on the airways of juvenile asthmatic rats, depending on the concentration. MHC1, MHC2, and VAV1 emerged as crucial mediators of these differential effects, suggesting their potential as targets for understanding sevoflurane's impact on asthmatic airways.
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