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<p>Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by neuronal loss and cognitive deficiency. Mitochondrial dysfunction and lysosomal abnormalities are critical during AD pathogenesis. The vesicular ATPase (v-ATPase) is a core regulator of lysosomal function, and its dysfunction impairs iron-sulfur protein synthesis and mitochondrial function. In this study, 4-month-old amyloid precursor protein/presenilin 1 (APP/PS1) double transgenic mice were treated with alkaloids from <i>Dendrobium nobile</i> Lindl (DNLA) at 20 and 40&#xa0;mg/kg/day via oral gavage for 5 months (<i>n</i> = 10 per group). The Y-maze test showed that DNLA alleviated cognitive dysfunction in APP/PS1 mice. HE, Nissl, and β-galactosidase staining indicated that DNLA mitigated brain damage. DNLA also increased the protein levels of v-ATPase subunits ATP6V1A and ATP6V0a1 in the cortex, promoted mitochondrial iron uptake and utilization, enhanced mitochondrial function, and reduced neuronal damage. Dendrobine (DDB) accounted for 84.6% in DNLA used for animal experiments, and purified DDB (99.7%) was applied for in vitro assays. In PC12 cells, DDB restored ATP6V1A expression, enhanced v-ATPase activity, delayed cellular senescence, improved iron utilization, and elevated mitochondrial membrane potential and ATP levels in ATP6V1A-knockdown cells. These findings suggest that DNLA may attenuate learning and memory impairment in APP/PS1 mice. The mechanism may be related to enhanced v-ATPase activity, promoted mitochondrial iron uptake and utilization, and improved mitochondrial function.</p>

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Alkaloids from Dendrobium Nobile Lindl Improves Mitochondrial Function by Enhancing the Activity of v-ATPase in APP/PS1 Mice

  • 期刊论文

  • 发表日期：

    2026年5月22日

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  • Qiye Li,
  • Yan Yang,
  • Bin Guo,
  • Xuejia Liu,
  • Guohui Luo,
  • Yajuan Wu,
  • Jing Nie

摘要

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by neuronal loss and cognitive deficiency. Mitochondrial dysfunction and lysosomal abnormalities are critical during AD pathogenesis. The vesicular ATPase (v-ATPase) is a core regulator of lysosomal function, and its dysfunction impairs iron-sulfur protein synthesis and mitochondrial function. In this study, 4-month-old amyloid precursor protein/presenilin 1 (APP/PS1) double transgenic mice were treated with alkaloids from Dendrobium nobile Lindl (DNLA) at 20 and 40 mg/kg/day via oral gavage for 5 months (n = 10 per group). The Y-maze test showed that DNLA alleviated cognitive dysfunction in APP/PS1 mice. HE, Nissl, and β-galactosidase staining indicated that DNLA mitigated brain damage. DNLA also increased the protein levels of v-ATPase subunits ATP6V1A and ATP6V0a1 in the cortex, promoted mitochondrial iron uptake and utilization, enhanced mitochondrial function, and reduced neuronal damage. Dendrobine (DDB) accounted for 84.6% in DNLA used for animal experiments, and purified DDB (99.7%) was applied for in vitro assays. In PC12 cells, DDB restored ATP6V1A expression, enhanced v-ATPase activity, delayed cellular senescence, improved iron utilization, and elevated mitochondrial membrane potential and ATP levels in ATP6V1A-knockdown cells. These findings suggest that DNLA may attenuate learning and memory impairment in APP/PS1 mice. The mechanism may be related to enhanced v-ATPase activity, promoted mitochondrial iron uptake and utilization, and improved mitochondrial function.