Background To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS. Methods In the present study, we established an in vitro ERS model using tunicamycin-treated hair-cell-like HEI-OC1 cells. The effect of dexamethasone on proliferation inhibition, apoptosis, and ATF4–CHOP pathway in HEI-OC1 cells was examined by CCK-8 assay, flow cytometry, western blotting, and reverse transcription PCR, respectively. Results In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist. Conclusion Dexamethasone can protect hair-cell-like HEI-OC1 cells from ERS damage, which may be one of the mechanisms of action for GCs in SNHL treatment.

中文翻译：

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糖皮质激素通过抑制内质网应激保护 HEI-OC1 细胞免受衣霉素诱导的细胞损伤

背景 为了分析糖皮质激素治疗感觉神经性听力损失 (SNHL) 中内质网应激 (ERS) 的作用机制，我们旨在评估蛋白激酶 RNA 样 ER 激酶 (PERK)–C/EBP 同源物的表达和激活状态。蛋白（CHOP）途径，这是 ERS ​​中的主要途径。方法 在本研究中，我们使用衣霉素处理的毛细胞样 HEI-OC1 细胞建立了体外 ERS ​​模型。分别通过 CCK-8 测定、流式细胞术、蛋白质印迹和逆转录 PCR 检测地塞米松对 HEI-OC1 细胞增殖抑制、凋亡和 ATF4-CHOP 通路的影响。结果 在 HEI-OC1 细胞中，地塞米松在持续存活和增殖的情况下显着降低衣霉素诱导的 ATF4 和 CHOP 表达，通过与糖皮质激素拮抗剂共同治疗可逆转的治疗效果。结论 地塞米松可以保护毛细胞样HEI-OC1细胞免受ERS损伤，这可能是GCs在SNHL治疗中的作用机制之一。