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<p>Alzheimer’s disease (AD) is a neurodegenerative disorder primarily affecting the elderly, characterized by mitochondrial dysfunction. Mitochondria play a dual role in AD, serving both as the main source of reactive oxygen species (ROS) generation and as a major target of oxidative damage. This study aimed to investigate the protective mechanisms of ellagic acid (EA) a natural dietary polyphenol on mitochondrial function in an intracerebroventricular (ICV) streptozotocin (STZ)-injected rat model of AD. Rats were randomly assigned to six groups: Control, Sham, STZ (1.5&#xa0;mg/kg on days 1 and 3), STZ + EA 5&#xa0;mg/kg, STZ + EA 50&#xa0;mg/kg, and STZ + EA 100&#xa0;mg/kg. On day 14, behavioral tests (Shuttle box and Step-down), histopathological evaluations, oxidative stress markers, and mitochondrial indices were assessed in brain tissue. Treatment with EA (100&#xa0;mg/kg) significantly improved spatial memory, as evidenced by increased latency time in the Morris water maze test (<i>p</i> &lt; 0.001). Furthermore, EA treatment mitigated hippocampal neurodegeneration, increasing neuronal density in the CA1 subfield (<i>p</i> &lt; 0.001) and restoring total hippocampal volume (<i>p</i> &lt; 0.01). At the biochemical level, EA markedly reduced oxidative stress levels (<i>p</i> &lt; 0.001) and enhanced mitochondrial function, restoring cortical ATP levels (<i>p</i> &lt; 0.001) and cytochrome c oxidase activity (<i>p</i> &lt; 0.01) compared to the STZ- group. In conclusion, these findings suggest that EA may have therapeutic potential in mitigating mitochondrial dysfunction and oxidative stress in AD, offering a promising approach for addressing neurodegeneration and energy deficits associated with the disease.</p>

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Mitochondrial protective effects of ellagic acid in a rat model of sporadic Alzheimer’s disease induced by STZ

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月26日

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  • Forouzan Khodaei,
  • Mohammad Reza Namavar,
  • Narges Soutodeh,
  • Arsalan Hadipour,
  • Freshteh Asadi,
  • Mohmmad Javad Khoshnoud,
  • Marzieh Rashedinia

摘要

Alzheimer’s disease (AD) is a neurodegenerative disorder primarily affecting the elderly, characterized by mitochondrial dysfunction. Mitochondria play a dual role in AD, serving both as the main source of reactive oxygen species (ROS) generation and as a major target of oxidative damage. This study aimed to investigate the protective mechanisms of ellagic acid (EA) a natural dietary polyphenol on mitochondrial function in an intracerebroventricular (ICV) streptozotocin (STZ)-injected rat model of AD. Rats were randomly assigned to six groups: Control, Sham, STZ (1.5 mg/kg on days 1 and 3), STZ + EA 5 mg/kg, STZ + EA 50 mg/kg, and STZ + EA 100 mg/kg. On day 14, behavioral tests (Shuttle box and Step-down), histopathological evaluations, oxidative stress markers, and mitochondrial indices were assessed in brain tissue. Treatment with EA (100 mg/kg) significantly improved spatial memory, as evidenced by increased latency time in the Morris water maze test (p < 0.001). Furthermore, EA treatment mitigated hippocampal neurodegeneration, increasing neuronal density in the CA1 subfield (p < 0.001) and restoring total hippocampal volume (p < 0.01). At the biochemical level, EA markedly reduced oxidative stress levels (p < 0.001) and enhanced mitochondrial function, restoring cortical ATP levels (p < 0.001) and cytochrome c oxidase activity (p < 0.01) compared to the STZ- group. In conclusion, these findings suggest that EA may have therapeutic potential in mitigating mitochondrial dysfunction and oxidative stress in AD, offering a promising approach for addressing neurodegeneration and energy deficits associated with the disease.