Effect of N-type acetylcholine receptor on inflammation in mouse model of acute respiratory distress syndrome
10.12007/j.issn.0258-4646.2025.02.007
- VernacularTitle:N型乙酰胆碱受体对急性呼吸窘迫综合征小鼠炎症反应的影响
- Author:
Zongbao YIN
1
;
Yanmei YU
1
;
Fan LIU
1
Author Information
1. 中南大学湘雅医学院附属海口医院急诊科,海口 570208
- Publication Type:Journal Article
- Keywords:
acute respiratory distress syndrome;
nicotinic acetylcholine receptor;
inflammation
- From:
Journal of China Medical University
2025;54(2):133-138
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of activating the N-type acetylcholine receptor(nAChR)on interleukin-18(IL-18)and PD-1 in mice with acute respiratory distress syndrome(ARDS).Methods Sixty healthy male BALB/c mice(6 weeks of age)were divided into six groups:normal(N),normal saline control(NS),normal saline+bilateral vagectomy(NS+D),ARDS+segmentation of the vagus nerve on both sides of the neck(A+D),ARDS(A),ARDS+vagal amputation,and administration of an acetylcholine receptor agonist(A+J)groups.Each group included ten mice that were fed and housed under normal conditions.Structural changes in the right lower lung were observed using fluorescence microscopy;phosphorylated nuclear factor-KB protein 65(p-NF-κBP65)levels were assessed using Western blotting;serum IL-18 and PD-1 levels were assessed using enzyme-linked immunosorbent assay(ELISA)and the double antibody sandwich method;and the percentages of CD3+and CD25+Foxp3+T lymphocytes in the middle lobe of right lung were determined using flow cytometry.Results No inflammatory cell infiltration was observed in groups N and NS.The interstitial lobes in groups A and A+D showed severe inflammatory infiltration,thickening of the alveolar wall,destruction of the alveolar structure,and loss of the alveolar cavity.Serum IL-18 and PD-1 levels in groups A and A+D were significantly higher than those in the other four groups(P＜0.05).p-NF-κBP65 and PD-1 levels in groups A and A+D were significantly higher than those in groups N,NS,and A+J(P＜0.05).CD3+and CD25+Foxp3+T cells in groups A and A+D were significantly higher than those in the other four groups(P＜0.05).Conclusion Active nAChR can inhibit IL-18 and p-NF-κBP65 through the negative regulation of T lymphocytes,decrease PD-1 expression in lung tissues,and alleviate the pathological changes of ARDS.
