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Background <p>Cadmium (Cd) is a well-established neurotoxic heavy metal. Several epidemiological studies have highlighted its involvement in the pathogenesis of Alzheimer’s disease (AD). AD is a multifactorial disorder influenced by environmental factors such as heavy metals. <i>Erythrina caffra</i> (<i>E. caffra</i>) is a medicinal plant rich in bioactive compounds with anti-inflammatory, antioxidant, and anticholinesterase properties. However, its protective potential against Cd-induced neurodegeneration remains insufficiently explored. This study investigated the effects of Cd on memory, cholinergic function, oxidative stress, and neuroinflammation, as key AD-related pathophysiological features, and evaluated the therapeutic potential of <i>E. caffra</i> seeds ethanolic extract.</p> Methods and Results <p>AD-like alterations were induced in Wistar rats by intracerebroventricular (ICV) administration of cadmium chloride (CdCl<sub>2</sub>). Animals were treated with <i>E. caffra</i> ethanolic extract (2.5&#xa0;mg/kg) or memantine (20&#xa0;mg/kg) by oral gavage. Behavioral, neurobiochemical, and histological analyses were performed to assess memory, cholinergic function, oxidative stress, neuroinflammation, and neuronal integrity. Cd exposure significantly impaired memory and disrupted cholinergic function, as evidenced by reduced acetylcholine (ACh) levels in the hippocampus. Moreover, it induced oxidative stress, marked by decreased catalase (CAT), superoxide dismutase (SOD), and non-protein thiols (NPSH), alongside increased proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and hippocampal neuronal loss. Treatment with <i>E. caffra</i> and memantine significantly ameliorated these alterations.</p> Conclusions <p><i>E. caffra</i> extract demonstrates neuroprotective effects against Cd-induced AD-like pathology by modulating oxidative stress, neuroinflammation, and cholinergic dysfunction. These findings suggest its potential as a promising therapeutic candidate for mitigating neurodegenerative processes associated with AD.</p>

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Erythrina caffra extract restores memory, modulates cholinergic dysfunction, neuroinflammation, and attenuates oxidative stress in cadmium-induced alzheimer’s disease-like pathology in rats

  • 期刊论文

  • 发表日期：

    2026年5月28日

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  • Soumia Ed-Day,
  • Fatima Ezzahra Kacimi,
  • Radia El Gui,
  • Latifa Didou,
  • Laila Ibouzine-Dine,
  • Chaimae El Kourchi,
  • Samira Boulbaroud,
  • Azzouz Haddan,
  • Hicham Harhar,
  • Fatima-Zahra Azzaoui

摘要

Background

Cadmium (Cd) is a well-established neurotoxic heavy metal. Several epidemiological studies have highlighted its involvement in the pathogenesis of Alzheimer’s disease (AD). AD is a multifactorial disorder influenced by environmental factors such as heavy metals. Erythrina caffra (E. caffra) is a medicinal plant rich in bioactive compounds with anti-inflammatory, antioxidant, and anticholinesterase properties. However, its protective potential against Cd-induced neurodegeneration remains insufficiently explored. This study investigated the effects of Cd on memory, cholinergic function, oxidative stress, and neuroinflammation, as key AD-related pathophysiological features, and evaluated the therapeutic potential of E. caffra seeds ethanolic extract.

Methods and Results

AD-like alterations were induced in Wistar rats by intracerebroventricular (ICV) administration of cadmium chloride (CdCl2). Animals were treated with E. caffra ethanolic extract (2.5 mg/kg) or memantine (20 mg/kg) by oral gavage. Behavioral, neurobiochemical, and histological analyses were performed to assess memory, cholinergic function, oxidative stress, neuroinflammation, and neuronal integrity. Cd exposure significantly impaired memory and disrupted cholinergic function, as evidenced by reduced acetylcholine (ACh) levels in the hippocampus. Moreover, it induced oxidative stress, marked by decreased catalase (CAT), superoxide dismutase (SOD), and non-protein thiols (NPSH), alongside increased proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and hippocampal neuronal loss. Treatment with E. caffra and memantine significantly ameliorated these alterations.

Conclusions

E. caffra extract demonstrates neuroprotective effects against Cd-induced AD-like pathology by modulating oxidative stress, neuroinflammation, and cholinergic dysfunction. These findings suggest its potential as a promising therapeutic candidate for mitigating neurodegenerative processes associated with AD.