维生素 C 可抑制 NLRP3 炎症小体的激活并延缓雄性 C57BL/6 小鼠老年性听力损失的发生

IF 2.5 4区医学 Q3 NEUROSCIENCES

Neuroscience Letters Pub Date : 2024-07-14 DOI:10.1016/j.neulet.2024.137897

Jinlan Liu , Yongfeng Si , Xiaoying Huang , Xinran Lin , Lingjuan Lu , Changlin Wu , Xuan Guan , Yunsheng Liang

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引用次数: 0

摘要

维生素 C 对老年性听力损失（即老花眼）的疗效仍有待商榷。另外，NOD 类受体家族含吡啶域 3（NLRP3）炎性体诱导的炎症也参与了老花眼的进展。本研究调查了维生素 C 对雄性 C57BL/6 小鼠老花眼和 NLRP3 炎性体的影响。结果表明，维生素 C 治疗可改善听力，减少炎症因子的产生，抑制 NLRP3 炎性体的激活，并降低 C57BL/6 小鼠耳蜗、下丘和听皮层的细胞膜线粒体 DNA（mtDNA）。根据这项研究，维生素 C 可通过减少线粒体 DNA 的释放、抑制听觉通路中 NLRP3 炎性体的激活来保护雄性 C57BL/6 老花眼小鼠的听觉功能。我们的研究为应用维生素 C 治疗老花眼提供了理论依据。

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Vitamin C inhibits NLRP3 inflammasome activation and delays the development of age-related hearing loss in male C57BL/6 mice

The efficacy of vitamin C in age-related hearing loss, i.e., presbycusis, remains debatable. On a separate note, inflammation induced by the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is involved in the progression of presbycusis. In this study, we investigated the effect of vitamin C on male C57BL/6 mice’s presbycusis and NLRP3 inflammasome. The results showed that vitamin C treatment improved hearing, reduced the production of inflammatory factors, inhibited NLRP3 inflammasome activation, and decreased cytosolic mitochondrial DNA (mtDNA) in the C57BL/6 mouse cochlea, inferior colliculus, and auditory cortex. According to this study, vitamin C protects auditory function in male C57BL/6 presbycusis mice through reducing mtDNA release, inhibiting the NLRP3 inflammasome activation in the auditory pathway. Our study provides a theoretical basis for applying vitamin C to treat presbycusis.

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来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

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