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<p>The neuroprotective effectiveness of natural substances against neuroinflammatory pathways linked to Alzheimer’s disease (AD) is still not well understood. In this study, we used both in vivo and in silico methods to assess the therapeutic potential of magnolol at dosages of 25 and 50&#xa0;mg/kg body weight in a rat model of AD produced by aluminium chloride (AlCl₃). Significant cognitive impairments, elevated levels of malondialdehyde (MDA), and increased expression of important neuroinflammatory mediators, including nuclear factor kappa-B (NF-κB), interleukin (IL-6), and interleukin-1β (IL-1β), were all brought on by exposure to AlCl₃. Magnolol treatment markedly reduced the levels of pro-inflammatory cytokines, lactate dehydrogenase (LDH), and nitric oxide (NO), improved cognitive function, and strengthened antioxidant defence systems as shown by increased glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities. Histopathological examination further validated Magnolol’s neuroprotective properties, showing decreased neuronal degeneration. Magnolol has substantial binding affinities for NF-κB, IL-6, and IL-1β, according to molecular docking and dynamic modelling studies, indicating that it can directly influence neuroinflammatory signalling pathways. Overall, these results show that magnolol has important neuroprotective effects by reducing oxidative stress and inhibiting important inflammatory mediators, underscoring its potential as an effective treatment option for AD.</p>

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Magnolol mitigates neuroinflammation via NF-κB/IL-6/IL-1β pathways in AlCl₃-induced Alzheimer’s disease: insights from in-vivo and in-silico investigations

  • 期刊论文

  • 发表日期：

    2026年7月8日

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  • Fangyu Lin,
  • Yue Teng

摘要

The neuroprotective effectiveness of natural substances against neuroinflammatory pathways linked to Alzheimer’s disease (AD) is still not well understood. In this study, we used both in vivo and in silico methods to assess the therapeutic potential of magnolol at dosages of 25 and 50 mg/kg body weight in a rat model of AD produced by aluminium chloride (AlCl₃). Significant cognitive impairments, elevated levels of malondialdehyde (MDA), and increased expression of important neuroinflammatory mediators, including nuclear factor kappa-B (NF-κB), interleukin (IL-6), and interleukin-1β (IL-1β), were all brought on by exposure to AlCl₃. Magnolol treatment markedly reduced the levels of pro-inflammatory cytokines, lactate dehydrogenase (LDH), and nitric oxide (NO), improved cognitive function, and strengthened antioxidant defence systems as shown by increased glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities. Histopathological examination further validated Magnolol’s neuroprotective properties, showing decreased neuronal degeneration. Magnolol has substantial binding affinities for NF-κB, IL-6, and IL-1β, according to molecular docking and dynamic modelling studies, indicating that it can directly influence neuroinflammatory signalling pathways. Overall, these results show that magnolol has important neuroprotective effects by reducing oxidative stress and inhibiting important inflammatory mediators, underscoring its potential as an effective treatment option for AD.