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

IF 3 4区医学 Q2 NEUROSCIENCES

Neural Plasticity Pub Date : 2022-01-01 DOI:10.1155/2022/1298692

Liang Gong, Biao Chen, Jingyuan Chen, Yongxin Li

{"title":"Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell.","authors":"Liang Gong, Biao Chen, Jingyuan Chen, Yongxin Li","doi":"10.1155/2022/1298692","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":null,"pages":null},"PeriodicalIF":3.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117069/pdf/","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neural Plasticity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2022/1298692","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 5

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.

Abstract Image

查看原文本刊更多论文

维生素C对新霉素诱导HEI-OC1听觉细胞凋亡的保护作用

耳毒性听力损失是由毛细胞通过活性氧(ROS)的过度产生和随之而来的细胞凋亡而死亡。我们研究了维生素C (VC)对新霉素诱导的HEI-OC1细胞损伤的影响及其抑制机制。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。在机制上，VC减少新霉素诱导的ROS生成，抑制细胞死亡，提高细胞活力。VC抑制新霉素诱导的细胞凋亡，改善新霉素可降低抗凋亡细胞Bcl-2的表达，抑制新霉素可增加促凋亡细胞Bax、caspase-3切割和caspase-8的表达。TUNEL标记显示VC阻断了新霉素诱导的细胞凋亡。进一步研究发现VC对新霉素诱导的毛细胞死亡的影响是通过干扰JNK活化和p38磷酸化。这些结果表明VC通过抑制ROS的产生，通过对抗新霉素诱导的细胞凋亡信号而抑制细胞死亡。因此，VC是抗新霉素诱导的HEI-OC1细胞耳毒性的潜在候选保护剂。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neural Plasticity NEUROSCIENCES-

CiteScore

6.80

自引率

0.00%

发文量

审稿时长

16 weeks

期刊介绍： Neural Plasticity is an international, interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology. Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic neuroscience, behavioral neuroscience, cognitive neuroscience, biological psychology, and biological psychiatry.