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<p>Pearls, formed from the nacreous layers of marine mollusks, have long been used in traditional medicine, yet the molecular basis of their bioactivity remains insufficiently characterized. Mitochondrial dysfunction is a central feature of Alzheimer’s disease (AD) pathology and represents a critical therapeutic target. Although nacre extract has been reported to improve cognitive impairment, its effects on mitochondrial function and biogenesis under amyloid-β (Aβ)-induced toxicity remain unclear. In this study, we examined the impact of nacre extract on mitochondrial activity in PC12 cells and in an Aβ-injected mouse model. Treatment with nacre extract significantly alleviated Aβ-induced mitochondrial dysfunction in PC12 cells, restoring membrane potential, ATP production, and the expression of mitochondrial biogenesis–related genes, including PPARγ and Nrf1. MitoBright LT staining demonstrated recovery of mitochondrial mass following extract administration. In vivo, we first isolated and identified a sulfated polysaccharide fraction from nacre extract, which significantly improved Aβ-induced memory impairment. In parallel, this fraction preserved mitochondrial function in the brains of Aβ-injected mice, as evidenced by maintained membrane potential, ATP levels, and hippocampal succinate dehydrogenase expression. Together, these findings demonstrate that nacre extract exerts neuroprotective effects through its sulfated polysaccharide fraction, highlighting its potential as a marine-derived therapeutic resource against AD-related neurodegeneration.</p>

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Neuroprotective Effect of Marine-Derived Nacre Extract against Aβ-Induced Toxicity via Preservation of Mitochondrial Function and Biogenesis

  • 期刊论文

  • 发表日期：

    2025年12月20日

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  • Zhao Yan,
  • Yamato Yotsuya,
  • Yasushi Hasegawa

摘要

Pearls, formed from the nacreous layers of marine mollusks, have long been used in traditional medicine, yet the molecular basis of their bioactivity remains insufficiently characterized. Mitochondrial dysfunction is a central feature of Alzheimer’s disease (AD) pathology and represents a critical therapeutic target. Although nacre extract has been reported to improve cognitive impairment, its effects on mitochondrial function and biogenesis under amyloid-β (Aβ)-induced toxicity remain unclear. In this study, we examined the impact of nacre extract on mitochondrial activity in PC12 cells and in an Aβ-injected mouse model. Treatment with nacre extract significantly alleviated Aβ-induced mitochondrial dysfunction in PC12 cells, restoring membrane potential, ATP production, and the expression of mitochondrial biogenesis–related genes, including PPARγ and Nrf1. MitoBright LT staining demonstrated recovery of mitochondrial mass following extract administration. In vivo, we first isolated and identified a sulfated polysaccharide fraction from nacre extract, which significantly improved Aβ-induced memory impairment. In parallel, this fraction preserved mitochondrial function in the brains of Aβ-injected mice, as evidenced by maintained membrane potential, ATP levels, and hippocampal succinate dehydrogenase expression. Together, these findings demonstrate that nacre extract exerts neuroprotective effects through its sulfated polysaccharide fraction, highlighting its potential as a marine-derived therapeutic resource against AD-related neurodegeneration.