| Summary: | Maha J Balgoon Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi ArabiaCorrespondence: Maha J Balgoon, Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia, Tel +966555762237, Email mbalgoon@kau.edu.saBackground: 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: Lepidium sativum, aluminum, neuroinflammation, antioxidant, Aβ, AchE, tau, TGFβ1
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