Airway hyperreactivity and
inflammation are important factors in the aggravation of lung function.
Suplatast tosilate (IPD) is a novel and unique anti‑asthma clinical compound. However, the mechanisms of IPD action in the inhibition of
asthma remain to be elucidated. The present study aimed to investigate the role of the GATA binding protein 3 (GATA‑3)/
interleukin (IL)‑5 signaling pathway in IPD‑induced inhibition of
asthma. Sprague‑Dawley rats were sensitized by
intraperitoneal injection with
ovalbumin (OVA) to establish an animal model of
asthma. IPD was administered continuously (C‑IPD) or at a later stage (L‑IPD).
Budesonide (BUD) was used as a positive control. Airway resistance and the expression of genes at the
mRNA and
protein levels were measured. Morphological changes in lung tissue and the percentage of eosinophils (EOS) in peripheral blood were observed and correlation analysis was performed. The results revealed that sensitization by OVA significantly increased airway resistance and the percentage of EOS in peripheral blood and induced significant inflammatory changes in lung tissue, as demonstrated by thick epithelium, goblet cell
hyperplasia and submucosal cell infiltration. In addition, sensitization by OVA was found to markedly upregulate IL‑5
mRNA and
protein expression. Airway resistance was found to positively correlate with the expression of IL‑5 in the rat lung tissues. Sensitization by OVA was also observed to markedly enhance GATA‑3
protein expression and GATA‑3 levels were found to positively correlate with airway resistance and IL‑5 levels. Similar to the effect of BUD, treatment with C‑IPD or L‑IPD was found to significantly attenuate OVA‑induced increases in airway resistance and the percentage of EOS in peripheral blood. Notably, treatment with C‑IPD or L‑IPD markedly reduced the OVA-induced expression of IL‑5 and GATA‑3. In the present study, IPD intervention was demonstrated to ameliorate airway hyperreactivity and
inflammation and the mechanisms may involve inhibition of the GATA‑3/IL‑5 signaling pathway.