Inhibition of macrophage migration inhibitory factor alleviates LPS-induced inflammation response of HEI-OC1 cells via suppressing NF-kappa B signaling

Background: Sudden sensorineural hearing loss (SSNHL) is acute and unexplained. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine in several inflammatory diseases. However, its role in SSNHL remains elusive. Methods: Lipopolysaccharide (LPS) was used to induce the inflammatory response of murine auditory cells, HEI-OC1. Silencing of MIF in HEI-OC1 cells was achieved by transfection of short hairpin RNA against MIF. 740Y-P and IMD0354 were used to stimulate the PI3K pathway and suppress the NF-kappa B pathway, respectively. RT-qPCR and western blotting were used to examine MIF and cyclooxygenase 2 (COX2) expression in LPS-treated HEI-OC1 cells. ELISA was employed to assess prostaglandin E2 (PGE2) concentrations. Results: MIF was upregulated in LPS-treated HEI-OC1 cells. MIF knockdown reduced PGE2 synthesis and COX2 expression in LPS-treated HEI-OC1 cells. Moreover, MIF knockdown suppressed activation of the PI3K/AKT and NF-kappa B pathway in LPS-treated HEI-OC1 cells. Additionally, inhibition of MIF decreased PGE2 production and COX2 expression via inactivation of the NF-kappa B pathway. Conclusion: Inhibition of MIF alleviated LPS-induced inflammation in HEI-OC1 cells via inactivating the NF-kappa B signaling, which might provide a better understanding for SSNHL development.