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
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
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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