Baicalin regulates the development of pediatric asthma via upregulating microRNA-103 and mediating the TLR4/NF-κB pathway.

Abstract

Pediatric asthma seriously endangers the well-being and health of children worldwide. Baicalin (BA) protects against diverse disorders, including asthma. Therefore, this study explored the mechanism of BA in pediatric asthma. The ovalbumin (OVA)-induced asthmatic mouse model was established to evaluate BA efficacy from aspects of oxidative stress, inflammation, blood cells in bronchoalveolar lavage fluid (BALF) and collagen deposition. Differentially expressed microRNAs (miRs) in BA-treated mice were analyzed. Effects of BA on PDGF-BB-induced smooth muscle cells (SMCs) were assessed. miR downstream mRNA and the related pathway were predicted and verified, and their effects on asthmatic mice were evaluated. BA effectively reversed OVA-induced oxidative stress and inflammation, as well as decreased the number of total cells, eosinophils and neutrophils in BALF, and collagen deposition. miR-103 was significantly upregulated after BA treatment. BA inhibited the abnormal proliferation of PDGF-BB-induced SMCs, which was prevented by miR-103 knockdown. miR-103 targeted TLR4 and regulated the extent of NF-κB phosphorylation. In vivo, miR-103 inhibition weakened the alleviating effects of BA on asthma, which was then reversed after silencing of TLR4. We highlighted that BA has the potency to halt the pediatric asthma progression via miR-103 upregulation and the TLR4/NF-κB axis inhibition.