Abstract
Recent studies show that airway epithelial barrier dysfunction is closely associated with allergic inflammation and asthma pathogenesis. Tripterine, a pentacyclic triterpenoid isolated from the plant family Celastraceae, possesses anti-inflammatory and anti-oxidant properties. Our study aimed to investigate the effects of tripterine on lipopolysaccharide (LPS)-induced airway epithelial barrier dysfunction and the molecular mechanism involved. Cell viability and apoptosis were evaluated by CCK-8 assay and flow cytometry, respectively. The mRNA expressions and secretion of interleukin (IL)-6, IL-8, IL-1β, and mucin 5AC (MUC5AC) were detected by qRT-PCR and ELISA, respectively. The changes of the Hippo pathway were examined by western blot analyses of phosphorylated yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ). Results showed that LPS treatment induced viability inhibition and apoptosis in lung bronchial epithelial cell line (16HBE) cells. Exposure to LPS increased the mRNA expression and concentrations of IL-6, IL-8, IL-1β, and MUC5AC in 16HBE cells. However, pretreatment with tripterine attenuated the effects of LPS on 16HBE cells. Tripterine inhibited LPS-induced activation of the Hippo pathway in 16HBE cells. Moreover, knockdown of YAP attenuated LPS-induced airway epithelial barrier dysfunction in 16HBE cells. In conclusion, tripterine attenuated LPS-induced airway epithelial barrier dysfunction through suppressing the Hippo pathway, providing new insight into the mechanism responsible for the effects of tripterine in asthma.