Protective effects of circPVT1 against D-galactose-induced senescence in HEI-OC1 auditory cells

Age-related hearing loss (ARHL) is a progressive, bilaterally symmetric sensorineural hearing disorder characterized by predominant high-frequency threshold elevation, and it represents the most prevalent chronic sensory impairment in the geriatric population worldwide. Circular RNA PVT1 (circPVT1) has been identified as an endogenous inhibitor of cellular senescence in multiple cell types, but its expression profile and functional role in auditory cell senescence remain unknown.

In this study, we established a D-galactose-induced senescence model in HEI-OC1 auditory cells. Quantitative real-time PCR (qRT-PCR) was used to detect circPVT1 expression levels. Cell Counting Kit-8 (CCK-8) assay, Western blot, flow cytometry and dihydroethidium (DHE) staining were performed to evaluate the effects of circPVT1 overexpression on cell viability, senescence marker expression, apoptosis and reactive oxygen species (ROS) production. circPVT1 expression was significantly downregulated in D-galactose-induced senescent HEI-OC1 cells. Overexpression of circPVT1 markedly preserved cellular viability, downregulated the senescence-associated protein p21, suppressed intracellular ROS overproduction, and attenuated D-galactose-induced apoptosis in HEI-OC1 cells.

These findings identify circPVT1 as a novel anti-senescence factor in auditory cells, which exerts protective effects against D-galactose-induced senescence via alleviating oxidative stress injury and apoptosis. Our work highlights circPVT1 as a potential candidate molecule for further in vivo validation of ARHL intervention.