The objective of this study was to investigate the inhibitory effect of miR-135a in regulating JAK/STAT signaling pathway on airway
inflammation in asthmatic mice. An
asthma model was established by sensitization and stimulation with
ovalbumin (OVA), and the corresponding
drug intervention was given from the day of stimulation by means of nasal drops.
Airway hyperresponsiveness was tested. The content of miR-135a in the lung tissue of mice was detected by RT-PCR. The pathological changes of lung tissue were evaluated by HE staining.
Tumor necrosis factor (TNF)-α,
interleukin (IL)-6,
IL-5, and eotaxin in bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA and immunohistochemistry, respectively. The expression of JAK/STAT signaling pathway-related
protein in lung tissue was detected by western blot. To further validate the effect of miR-135a overexpression on the JAK/STAT signaling pathway, pathway activators and inhibitors were added. Compared with the OVA group, the
airway hyperresponsiveness of the mice was significantly decreased
after treatment with the miR-135a agonist. The expression of miR-135a was significantly increased in the lung tissue and the pathological changes of the lung tissue were alleviated. The contents of TNF-α,
IL-6,
IL-5, and eotaxin in BALF and lung tissues were decreased. The expression of JAK/STAT signaling pathway-related
proteins p-JAK3/JAK3, p-STAT1/STAT1, and p-STAT3/STAT3 were significantly reduced in lung tissue (P<0.05). Addition of
JAK inhibitor AG490 reduced airway
inflammation in asthmatic mice. miR-135a agonists inhibit airway
inflammation in asthmatic mice by regulating the JAK/STAT signaling pathway.