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Protective Effects of Vitamin C against Neomycin-Induced Apoptosis in HEI-OC1 Auditory Cell
Liang Gong1, Biao Chen1, Jingyuan Chen1
1Department of Otorhinolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100005, China.
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.
Insights
Vitamin C (VC) protects against neomycin-induced ototoxicity by reducing reactive oxygen species (ROS) and inhibiting apoptosis in hair cells. This suggests VC as a potential therapeutic agent for preventing hearing loss.
Area of Science:
- Oto-toxicology
- Cell Biology
- Biochemistry
Background:
- Ototoxic hearing loss stems from hair cell death driven by excessive reactive oxygen species (ROS) and apoptosis.
- Neomycin is a common ototoxic agent that induces hair cell damage.
Purpose of the Study:
- To investigate the protective effects of vitamin C (VC) against neomycin-induced damage in HEI-OC1 cells.
- To elucidate the underlying inhibitory mechanisms of VC.
Main Methods:
- HEI-OC1 cells were exposed to neomycin and/or vitamin C.
- Assessed cell viability, ROS generation, apoptosis markers (Bcl-2, Bax, caspase-3, caspase-8), and signaling pathways (JNK, p38).
- TUNEL labeling was used to confirm apoptosis inhibition.
Main Results:
- Vitamin C demonstrated a protective effect against neomycin-induced HEI-OC1 cell death.
- VC significantly decreased ROS generation, suppressed apoptosis, and enhanced cell viability.
- VC modulated apoptotic markers, inhibiting proapoptotic proteins and restoring antiapoptotic expression, while also interfering with JNK and p38 activation.
Conclusions:
- Vitamin C mitigates neomycin-induced ototoxicity by suppressing ROS production and counteracting apoptotic signaling pathways.
- VC shows potential as a protective agent against neomycin-induced hair cell damage and subsequent ototoxicity.
