Expressions of cav-1 and TNF-α in mechanical ventilation combined with hyperoxia induced ALI rats

Abstract

Objective To observe the expressions of caveolin-1 (cav-1), nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α) in mechanical ventilation combined with hyperoxia induced acute lung injury rats, and explore the mechanism and interaction of acute lung injury induced by mechanical ventilation combined with hyperoxia. Methods 24 male SD rats were randomly divided into control group, mechanical ventilation group (MV group) and mechanical ventilation combined with hyperoxia group (MV+ HO2 group). The pathological changes of lung tissues were observed and lung wet/dry weight ratio was calculated.The concentration of protein in bronchoalveolar lavage fluid (BALF) was tested by BCA method.The expression of cav-1 protein in lung tissue was tested by immunohistochemistry and Western blot method.The expressions of NF-κB and TNF-α mRNA in lung tissue were tested by RT-qPCR. Results Compared with the control group, the lung wet/dry weight ratio, the level of total protein in BALF, the expressions of cav-1 protein, NF-κB mRNA and TNF-α mRNA in lung tissues were significantly increased (all P<0.001), and lung tissue was obviously changed in MV group and MV+ HO2 group.There were significant differences between MV group and MV+ HO2 group in the above indexes (all P<0.001), but the degree of pathological damage of lung tissue in MV group was lighter than that in MV+ HO2 group.Correlation analysis showed that the expression of cav-1 in the lung tissue of each group was positively correlated with the expression of NF-κB mRNA(r=0.827, P<0.001), NF-κB mRNA expression and TNF-α mRNA expression was positively correlated (r=0.903, P<0.001). Conclusions Hyperoxia can upregulate cav-1 expression in lung tissue and make NF-κB signaling pathway activation, which can increase the inflammatory injury of lung tissue in mechanical ventilation rats by release of inflammatory cytokines, such as TNF-α. Key words: Cavolin-1; Tumor necrosis factor-α; Nuclear factor-κB; Acute lung injury