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维生素 C 对庆大霉素诱导的 HEI-OC1 听觉细胞凋亡的保护作用。

Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell.

机构信息

Department of Otorhinolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100005, China.

出版信息

Neural Plast. 2022 May 11;2022:1298692. doi: 10.1155/2022/1298692. eCollection 2022.

DOI:10.1155/2022/1298692
PMID:35601667
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9117069/
Abstract

Ototoxic hearing loss results from hair cell death via reactive oxygen species (ROS) overproduction and consequent apoptosis. We investigated the effects of vitamin C (VC) on neomycin-induced HEI-OC1 cell damage, as well as the mechanism of inhibition. HEI-OC1 cells were treated with neomycin or with vitamin C (VC). The results indicated that VC had a protective effect on neomycin-induced HEI-OC1 cell death. Mechanistically, VC decreased neomycin-induced ROS generation, suppressed cell death, and increased cell viability. VC inhibited neomycin-induced apoptosis, ameliorated neomycin reduced antiapoptotic Bcl-2 expression, and suppressed neomycin increased expression of proapoptotic Bax, caspase-3 cleavage and caspase-8. TUNEL labeling demonstrated that VC blocked neomycin-induced apoptosis. Further study revealed that the effect of VC on neomycin-induced hair cell death was through interference with JNK activation and p38 phosphorylation. These results indicate that VC via suppressed ROS generation, which inhibited cell death by counteracting apoptotic signaling induced by neomycin in cells. Hence, VC is a potential candidate for protection agent against neomycin-induced HEI-OC1 cell ototoxicity.

摘要

耳毒性听力损失是由于毛细胞通过活性氧（ROS）过度产生和随后的细胞凋亡而死亡引起的。我们研究了维生素 C（VC）对新霉素诱导的 HEI-OC1 细胞损伤的影响，以及抑制的机制。用新霉素或维生素 C（VC）处理 HEI-OC1 细胞。结果表明，VC 对新霉素诱导的 HEI-OC1 细胞死亡具有保护作用。从机制上讲，VC 减少了新霉素诱导的 ROS 生成，抑制了细胞死亡，增加了细胞活力。VC 抑制了新霉素诱导的细胞凋亡，改善了新霉素降低的抗凋亡 Bcl-2 表达，并抑制了新霉素增加的促凋亡 Bax、caspase-3 切割和 caspase-8。TUNEL 标记表明 VC 阻断了新霉素诱导的细胞凋亡。进一步的研究表明，VC 对新霉素诱导的毛细胞死亡的作用是通过干扰 JNK 激活和 p38 磷酸化来实现的。这些结果表明，VC 通过抑制 ROS 的产生，通过抵消新霉素诱导的细胞凋亡信号来抑制细胞死亡。因此，VC 是对抗新霉素诱导的 HEI-OC1 细胞耳毒性的潜在候选保护剂。

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