Effect of carbachol on lung injury induced by hyperoxia in mice
10.3760/cma.j.issn.1671-0282.2019.01.011
- VernacularTitle:卡巴胆碱对高氧诱导小鼠肺损伤的作用
- Author:
Zhe ZHANG
1
;
Dawei CAO
;
Huiqing SHEN
;
Mingxia HOU
;
Xinri ZHANG
Author Information
1. 山西医科大学第一医院呼吸与危重症医学科
- Keywords:
Hyperoxia;
Acute lung injury;
TLR4;
NF-κB;
Mice;
Signaling pathway
- From:
Chinese Journal of Emergency Medicine
2019;28(1):56-60
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of Carbachol on hyperoxia-induced acute lung injury (HALI) in mice and its related mechanisms. Methods Thirty-two healthy male ICR mice were randomly divided into four groups:control group, hyperoxia exposure three days group (HO3d group), hyperoxia exposure three days + Carbachol group (HO3d+Carba group), and Carbachol group (Carba group), eight mice in each group. The pathological changes of lung tissue in each group were observed under light microscope after the models were completed in each group.The expression of TLR4 and NF-κB protein in lung tissues were detected by Western blot, and the expression of HMGB-1 and TNF-α mRNA in lung tissues by RT-PCR. LSD-t test was used for sample pairwise comparison, and one-way ANOVA for intergroup comparison. P<0.05 was considered statistically significant. Results There was no statistical difference between the control group and the Carba group (P> 0.05), and no obvious abnormal changes in lung tissue structure. The expression of TLR4, NF-κB protein and HMGB-1 and TNF-α mRNA in the HO3d group were significantly higher than those in the control group (P<0.01), and there were obvious bleeding on the surface of the lung tissue and severe pathological damage. The expression of TLR4,NF-κB protein and HMGB-1 and TNF-α mRNA in the HO3d+Carba group were significantly lower than those in the HO3d group(P<0.01), while lung tissue damage degree was also lower than that in the HO3d group. Conclusions Hyperoxia can increase the expression of TLR4 and NF-κB in lung tissues, and cause inflammatory injury in lung tissue. Carbachol can reduce the release of HMGB-1 and TNF-α inflammatory factors in hyperoxia-induced acute lung injury, and its mechanism is related to the inhibition of TLR4/NF-κB signal pathway, which has a protective effect on HALI.
