抑制巨噬细胞移动抑制因子通过抑制 NF-κB 信号通路减轻 LPS 诱导的 HEI-OC1 细胞炎症反应。
Inhibition of macrophage migration inhibitory factor alleviates LPS-induced inflammation response of HEI-OC1 cells via suppressing NF-κB signaling.
机构信息
Department of Otolaryngology-Head and Neck Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu 223300, China.
Department of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China.
出版信息
Cytokine. 2022 Feb;150:155776. doi: 10.1016/j.cyto.2021.155776. Epub 2021 Dec 1.
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-κB 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-κB pathway in LPS-treated HEI-OC1 cells. Additionally, inhibition of MIF decreased PGE2 production and COX2 expression via inactivation of the NF-κB pathway.
CONCLUSION
Inhibition of MIF alleviated LPS-induced inflammation in HEI-OC1 cells via inactivating the NF-κB signaling, which might provide a better understanding for SSNHL development.
背景
突发性聋是一种急性、原因不明的听力损失。巨噬细胞移动抑制因子（MIF）是多种炎症性疾病中的一种促炎细胞因子。然而，其在突发性聋中的作用仍不清楚。
方法
脂多糖（LPS）用于诱导小鼠听觉细胞 HEI-OC1 的炎症反应。通过针对 MIF 的短发夹 RNA（shRNA）转染来沉默 HEI-OC1 细胞中的 MIF。740Y-P 和 IMD0354 分别用于刺激 PI3K 通路和抑制 NF-κB 通路。RT-qPCR 和 Western blot 用于检测 LPS 处理的 HEI-OC1 细胞中 MIF 和环氧化酶 2（COX2）的表达。ELISA 用于评估前列腺素 E2（PGE2）浓度。
结果
LPS 处理的 HEI-OC1 细胞中 MIF 上调。MIF 敲低减少了 LPS 处理的 HEI-OC1 细胞中 PGE2 的合成和 COX2 的表达。此外，MIF 敲低抑制了 LPS 处理的 HEI-OC1 细胞中 PI3K/AKT 和 NF-κB 通路的激活。此外，通过抑制 NF-κB 通路，抑制 MIF 减少了 PGE2 的产生和 COX2 的表达。
结论
抑制 MIF 通过抑制 NF-κB 信号通路减轻 LPS 诱导的 HEI-OC1 细胞炎症，这可能为突发性聋的发展提供更好的理解。
Zotero 插件