Abstract
It has been reported that the expression of C-X-C motif chemokine receptor 4 (CXCR4) is increased in patients with lung injury, while CXCR4 downregulation can improve sepsis-induced lung injury. Previous studies have shown that tranilast can inhibit CXCR4 mRNA expression. Therefore, the present study aimed to investigate whether tranilast could protect against lipopolysaccharide (LPS)-induced lung injury via the CXCR4/Janus kinase 2 (JAK2)/STAT3 signaling pathway. A Cell Counting Kit-8 assay was performed to evaluate the effect of different concentrations of tranilast on the viability of LPS-induced BEAS-2B cells. The mRNA and protein expression levels of the inflammatory factors, TNFα, IL-1β, IL-6, cytochrome c oxidase subunit II and inducible nitric oxide synthase were detected using reverse transcription-quantitative PCR and western blot analysis, respectively. In addition, the cell apoptosis rate and the expression levels of apoptosis-related proteins were analyzed using a TUNEL staining assay and western blot analysis, respectively. The expression levels of the CXCR4/JAK2/STAT3 signaling pathway-related proteins were also determined using western blot analysis. Furthermore, the effects of tranilast on cell viability, inflammation and apoptosis were also evaluated in LPS-stimulated BEAS-2B cells following CXCR4 overexpression, which were pre-treated with tranilast. The results demonstrated that tranilast could alleviate LPS-induced cell viability, the secretion of inflammatory cytokines and cell apoptosis. In addition, cell treatment with tranilast inhibited the expression of CXCR4/JAK2/STAT3 signaling-related proteins in LPS-induced BEAS-2B cells. Following CXCR4 overexpression, the alleviating effect of tranilast on cell viability, inflammatory response and apoptosis was notably attenuated. Overall, the current study suggested that tranilast could attenuate LPS-induced lung injury via the CXCR4/JAK2/STAT3 signaling pathway, suggesting that tranilast could be considered as a promising agent for treating sepsis-induced acute lung injury.
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