Background: Bioaccumulation of aluminum in the brain is associated with adverse neuroinflammatory and neurodegenerative changes, such as those seen in Alzheimer's disease (AD).
Objective: This study aimed to assess the impact of the administration of Lepidium sativum (LS) extract on behavioral, biochemical, and cerebral histopathological changes in rats with AlCl3-induced AD and explore the mechanism behind this effect.
Materials and methods: This study was conducted on 40 male albino rats divided into four groups (n=10): LS (control, 20 mg/kg body weight for 8 weeks), AD (AlCl3, 10 mg/kg body weight), and an LS-treated AD group. Behavioral assessment included radial armed maze and active avoidance training tests. Proinflammatory cytokines, oxidant/antioxidant markers, Aβ, AchE, tau protein, TGFβ1, homocysteine, folic acid, and vitamin B12 were biochemically assessed in the serum. The cerebral cortex was histopathologically examined.
Results: AlCl3 administration significantly impaired rats' memory, indicating AD-like behavioral changes, significantly increased (P<0.001) oxidative stress markers, enhanced proinflammatory cytokines, and significantly increased AChE (P<0.001) adding to cytotoxic effects and neuronal loss in the cerebral cortex. LS administration significantly improved the antioxidant parameters, reduced proinflammatory cytokines, and alleviated AD-associated histopathological changes.
Conclusion: LS ameliorated AlCl3-induced changes through its antioxidant, anti-inflammatory, and antiapoptotic effects, suggesting that it has a neuroprotective effect.
Keywords: AchE; Aβ; Lepidium sativum; TGFβ1; aluminum; antioxidant; neuroinflammation; tau.
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