The neurotoxicity of β-amyloid peptide toward rat brain is associated with enhanced oxidative stress, inflammation and apoptosis, all of which can be attenuated by scutellarin

Abstract

This study was designed to investigate the processes underlying the neurotoxicity induced by β-amyloid peptide (Aβ) in the rat brain, as well as to examine whether scutellarin (Scu) can prevent this neurotoxicity. Thirty Wistar rats were randomly divided into 3 groups, i.e., untreated (control), treated with Aβ and treated with both Aβ and Scu. The treated rats were subjected to bilateral intracerebroventricular injection of Aβ(25-35) with or without subsequent dietary exposure to Scu. Learning and memory were assessed with the Morris water maze test; the activities of superoxide dismutase (SOD) and monoamine oxidase (MAO) were assayed biochemically; expression of the interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) proteins was determined by immunohistochemistry; and neuronal apoptosis was detected with Annexin staining followed by flow cytometry. The animals treated with Aβ exhibited impaired learning and memory; reduced SOD and elevated MAO activity, elevated protein levels of IL-1β, IL-6 and TNF-α; and a higher percentage of apoptotic neurons in the brain. Interestingly, all of these effects were ameliorated by administration of Scu. These findings indicate that the deficits in learning and memory demonstrated by the rats receiving Aβ are due to elevated oxidative stress and inflammation, which result in apoptosis and that Scu may prevent these deleterious effects.