Scholarlink

<p>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<sub>2</sub>O<sub>2</sub>) 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<sub>2</sub>O<sub>2</sub>) 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<sub>2</sub>O<sub>2</sub>-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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月2日

查看全文
  • Yongqing Ding,
  • Yachao Liu,
  • Dong Li,
  • Ruili Hu,
  • Zedong Tian,
  • Lihang Yang,
  • Yanping Li,
  • Yantao Lin,
  • Yan Qu

摘要

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 (H2O2) 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 (H2O2) 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 H2O2-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.