Melatonin Ameliorates Senescence of Mouse Auditory Cell Line HEI-OC1 Cells by Suppressing NLRP3 Inflammasome-Mediated Pyroptosis.

The aim of this study was to determine whether oxidative stress-induced premature senescence in mouse auditory cell line HEI-OC1 cells in vitro is associated with NLRP3 inflammasome activation and pyroptosis, and whether melatonin has a protective effect. HEI-OC1 cells were exposed to different concentrations of hydrogen peroxide (H(2)O(2)) to induce oxidative stress and subsequently analyzed by Western blotting to measure pyroptosis-related proteins - NLRP3, caspase-1, and GSDMD-N. Compared with untreated control cells, exposure to different concentrations of hydrogen peroxide (H(2)O(2)) promoted premature senescence of HEI-OC1 cells, accompanied by a significant increase in levels of pyroptosis-related proteins - NLRP3, caspase-1, and GSDMD-N. Furthermore, melatonin treatment was shown to decrease the expression of these proteins in HEI-OC1 cells and attenuate the H(2)O(2)-induced senescence process. NLRP3 inflammasome activation contributes to oxidative stress-induced premature senescence of HEI-OC1 cells in vitro, leading to pyroptosis. Melatonin attenuates pyroptosis and senescence in HEI-OC1 cells by inhibiting the expression of NLRP3, caspase-1, and GSDMD-N, providing reliable evidence for melatonin as a potential therapeutic agent for age-related hearing loss.