ArticleMolecular biology reports2024
Vitamin C ameliorates D-galactose-induced senescence in HEI-OC1 cells by inhibiting the ROS/NF-κB pathway.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Gut-Metabolome-Proteome Interactions in Age-Related Hearing Loss: Insights from Fecal Microbiota Transplantation and Multi-Omics Analyses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Engineered Inner Ear Drug Delivery Systems for Hearing Loss Treatment.Research (Washington, D.C.) · 2026Review
- Aspirin in Audiology: A Dual-Edged Sword in Hearing Loss and Its Nanotechnology-Driven Future.Drug design, development and therapy · 2026Review
- A modified system to promote stemness of mouse intestinal stem cells by activating Nrf2 and α2-adrenergic receptor signaling pathway.Acta biochimica et biophysica Sinica · 2025Article
- Bibliometric analysis and initial animal efficacy evaluation of top ten scoring drugs to enhance oral rehydration therapy in early post-burn shock.Frontiers in pharmacology · 2025Article
- A Human Embryonic Stem Cell-derived Neural Stem Cell Senescence Model Triggered by Oxidative Stress.Current stem cell research & therapy · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCochlear hair cell senescence is one of the major causes of age-related hearing loss (ARHL) and is significantly related to reactive oxygen species (ROS) accumulation. Research shows that vitamin C (VC) can inhibit ROS accumulation; however, its association with cochlear hair cell senescence remains elusive. METHODS AND
resultsFirstly, a cellular senescence model was established using D-galactose (D-gal) induced HEI-OC1 cells for 24 h. Senescent HEI-OC1 cells were then continued to be treated with the addition of VC or ROS inhibitor (N-acetylcysteine; NAC) for another 24 h, and explored the impact of VC on senescent cochlear hair cell and the potential regulatory mechanisms. The results indicated that D-gal-induced senescent HEI-OC1 cells, manifested as decreased cell viability, increased β-galactosidase activity and p21 protein level, and ROS and pro-inflammatory factors were upregulated, and NF-κB p65 phosphorylation was enhanced. However, the use of VC or NAC can significantly ameliorate these effects and improve HEI-OC1 cell senescence.
conclusionsThis research indicates that VC can ameliorate D-gal-induced senescence of HEI-OC1 cochlear hair cells, and its protective effect may be related to the inhibition of the ROS/NF-κB pathway, which provides a new research direction for the prevention and treatment of ARHL.
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Registered trials
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