Objective: To explore the expression and significance of miR-223 in mice with pulmonary fibrosis.
Materials and methods: The rats were separated into a control group (n=15), a sham operation group (n=15), and a model group (n=45) (which was then divided into a 3-day group, a 7-day group, and a 14-day group, with 15 rats in each group). The rat model of pulmonary fibrosis was established. The rats in the model group were injected with bleomycin solution, while those in the control group and sham operation group were given the same operation and injected with the same amount of normal saline. After observing the pulmonary function indexes of the rats on the 3rd, 7th and 14th days after modeling, the rats were sacrificed by cervical dislocation, the pulmonary inflammation and fibrosis of the rats were observed, and the HYP (hydroxyproline) content and miR-223 expression level were determined. Pearson correlation analysis was employed to analyze the correlation between miR-223 and HYP.
Results: The pulmonary inflammation score of the model group was significantly higher than that of the sham group and the control group, and the pulmonary inflammation of the model group significantly increased with the increase of time (p<0.05). The pulmonary fibrosis score in the model group was markedly higher than that in the rest two groups, and the pulmonary fibrosis in the model group elevated significantly with the passage of time (p<0.05). The relevant pulmonary function indexes of the model group rats were significantly lower than those of the other two groups, and the pulmonary function of the model group rats gradually decreased with time (p<0.05). As to the HYP, it presented notably higher content in the model group than in the remaining two groups, and its content in the model group rats increased significantly with time (p<0.05). The expression of miR-223 decreased with the increase of fibrosis (p<0.05), and the expression level of miR-223 was negatively correlated with the HYP content (p<0.05).
Conclusions: MiR-572 targeted CDH1 to promote cell metastasis in WT by suppressing EMT.