Effects of α7nAChR on CD11b and inflammatory cytokines in mice with acute respiratory distress syndrome
- Author:
SUN Qiong
;
YU Yanmei
;
LIU Fan
;
YIN Zongbao
- Publication Type:Journal Article
- Keywords:
α7 nicotinic acetylcholine receptor;
CD11b;
interleukin-1β;
interleukin-18;
tumor necrosis factor-α
- From:
China Tropical Medicine
2024;24(1):82-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of α7 nicotinic acetylcholine receptor (α7nAChR) on CD11b, IL-1β, IL-18 and TNF-α in acute respiratory distress syndrome (ARDS) mice. Methods A total of 40 healthy and clean male Balb/C mice (6 weeks old) were randomly divided into normal group (N group), normal saline control group (NS group), ARDS group (A group), and ARDS mice treated with nicotinic acetylcholine receptor agonist after bilateral cervical vagotomy group (J group), with 10 mice in each group. The right lung structure of mice in each group was observed by hematoxylin-eosin (HE) staining, the lung tissue wet weight/body weight ratio (LWW/DW ratio) was detected, and the percentage of CD11b in the alveolar lavage fluid of mice was detected by flow cytometry. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of IL-1β mRNA, IL-18 mRNA and TNF-α mRNA in left lung tissue. Serum IL-18 was determined by enzyme-linked immunosorbent assay (ELISA) and double antibody sandwich method. Results HE staining of the right lung of mice in group N and NS showed normal structure, while the lung interstitial of mice in group A showed a large number of inflammatory cells infiltrated, alveolar wall thickened, alveolar structure destroyed and alveolar cavity fused. The alveolar structure of mice in group J was intact, with a little damage and alveolar cavity. The percentage of CD11b in alveolar lavage fluid in group A was higher than that in the other three groups, and the difference was statistically significant compared with group N, NS and J, respectively (P<0.05). The expressions of IL-1β mRNA, IL-18 mRNA and TNF-α mRNA in the left lung of mice in group J were statistically significant compared with those in group N, NS and A (P<0.05), and the serum IL-18 level of mice in group A was higher than that in the other three groups, and the differences were statistically significant compared with groups N, NS and J, respectively (P<0.05). Conclusions Activation of α7nAChR can directly inhibit the release of CD11b in lung tissue and reduce the accumulation of inflammatory factors. Simultaneously, it can also directly inhibit the expression of IL-β1 mRNA, IL-18 mRNA and TNF-α mRNA in lung tissue and the release of IL-18, thus inhibiting the inflammatory response of ARDS and alleviating the pathological changes of ARDS.
- Full text:202502191001410895815.Effects of α7nAChR on CD11b and inflammatory cytokines in mice with acute respiratory distress syndrome.pdf
