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Background <p>Alzheimer’s disease (AD) is characterized by amyloid-β (Aβ) deposition, which triggers oxidative stress and neuronal damage. Atractylenolide III (AT-III), a plant-derived monomer with antioxidant properties, has shown promise but its neuroprotective effects in AD remain unclear.</p> Methods <p>We established an AD mice model via intracerebroventricular Aβ₁₋₄₂ injection and evaluated AT-III’s neuroprotective effects using behavioral tests, electrophysiological recordings, Western blot, and ELISA. Additionally, we assessed AT-III’s protective effects against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative stress in Neuro-2&#xa0;A (N2A) cells.</p> Results <p>AT-III mitigated cognitive and long-term potentiation (LTP) deficits induced by Aβ<sub>1−42</sub>. It also reduced oxidative stress by decreasing pro-oxidants and increasing anti-oxidants. Furthermore, AT-III activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in the model mice, consequently enhancing the expression of Nrf2, heme oxygenase-1 (HO-1), and superoxide dismutase-1 (SOD-1). In N2A cells, AT-III significantly attenuated H<sub>2</sub>O<sub>2</sub>-induced cytotoxicity and oxidative stress, further supporting its role in neuroprotection.</p> Conclusions <p>These results suggest that AT-III may exert neuroprotective effects through antioxidant properties, thereby ameliorating cognitive impairment induced by Aβ<sub>1−42</sub>. These findings indicate that AT-III could be a potential therapeutic agent for AD.</p>

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Atractylenolide III alleviates amyloid-β-induced cognitive impairments in mice

  • 期刊论文

  • 发表日期：

    2025年8月7日

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  • Hao Yuan,
  • Lei Xia,
  • Junjie Li,
  • Chunfang Dai,
  • Xiaohuan Li,
  • Boqing Xu,
  • Mengtong Xue,
  • Xiuyu Shi,
  • Bin Wu,
  • Zhifang Dong,
  • Yayan Pang

摘要

Background

Alzheimer’s disease (AD) is characterized by amyloid-β (Aβ) deposition, which triggers oxidative stress and neuronal damage. Atractylenolide III (AT-III), a plant-derived monomer with antioxidant properties, has shown promise but its neuroprotective effects in AD remain unclear.

Methods

We established an AD mice model via intracerebroventricular Aβ₁₋₄₂ injection and evaluated AT-III’s neuroprotective effects using behavioral tests, electrophysiological recordings, Western blot, and ELISA. Additionally, we assessed AT-III’s protective effects against hydrogen peroxide (H2O2)-induced oxidative stress in Neuro-2 A (N2A) cells.

Results

AT-III mitigated cognitive and long-term potentiation (LTP) deficits induced by Aβ1−42. It also reduced oxidative stress by decreasing pro-oxidants and increasing anti-oxidants. Furthermore, AT-III activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in the model mice, consequently enhancing the expression of Nrf2, heme oxygenase-1 (HO-1), and superoxide dismutase-1 (SOD-1). In N2A cells, AT-III significantly attenuated H2O2-induced cytotoxicity and oxidative stress, further supporting its role in neuroprotection.

Conclusions

These results suggest that AT-III may exert neuroprotective effects through antioxidant properties, thereby ameliorating cognitive impairment induced by Aβ1−42. These findings indicate that AT-III could be a potential therapeutic agent for AD.