Abstract
Scrophularia buergeriana (SB) Miq. (Scrophulariaceae) has been used to help cure swelling and fever and has reported antioxidant and neuro-protective effects. However, few mechanism–based studies have evaluated the memory-improving effects in a beta-amyloid induced memory loss model. As a result of Scrophularia buergeriana extract (SBE) administration (30 and 100 mg/kg) for 28 days significantly recovered beta-amyloid-induced amnesia in the passive avoidance test and improved the impairment of spatial memory in the Morris Water Maze (MWM) task. Furthermore, SBE up-regulated superoxide dismutase-1 (SOD)-1, SOD-2, glutathione peroxidase-1, and B-cell lymphoma (Bcl)-2 protein expression levels. Additionally, SBE downregulated Bcl-2-associated X protein, cleaved caspase-9, cleaved poly (adenosine diphosphate-ribose) polymerase, and Aβ protein expression levels and inhibited the phosphorylation of the tau protein of Aβ-treated mice hippocampus. These results demonstrate that SBE improved memory impairment by reducing beta-amyloid induced neurotoxicity and regulated oxidative stress, anti-apoptotic pathways.
Highlights
Alzheimer’s disease (AD) is one type of dementia and a progressive neuro-degenerative disease featured by deposits of extracellular amyloid β (Aβ) peptide and flame-shaped neurofibrillary tangles of hyper-phosphorylated tau protein, inducing neurotoxicity accompanied by cognitive impairment and memory loss [1,2,3,4]
Aβ-injected mice demonstrated a remarkable reduction in the time to move from the illuminated compartment to the shaded area compared to normal mice (p < 0.01), implying that the learning capacity was lowered
We have demonstrated that neuronal cell death and cognitive deficiency due to oxidative stress are related to Aβ accumulation in the brain
Summary
Alzheimer’s disease (AD) is one type of dementia and a progressive neuro-degenerative disease featured by deposits of extracellular amyloid β (Aβ) peptide and flame-shaped neurofibrillary tangles of hyper-phosphorylated tau protein, inducing neurotoxicity accompanied by cognitive impairment and memory loss [1,2,3,4].The Aβ plaque is composed of Aβ 1–40 and 1–42, major forms of Aβ found in the brains of AD patients. The Aβ 1–42 protein is more neurotoxic and induces more oxidative damage than Aβ 1–40 [5]. An important factor in AD development is considered to be Aβ accumulation, since oxidative stress is followed by Aβ cytotoxicity [1,6]. Aβ accumulation and oxidative stress damages cellular components resulting in structural damage, functional disorder, and cell apoptosis [7]. SOD is known as the first detoxification enzyme and the most powerful endogenous antioxidant in the cell. It acts as a catalyst and converse of the superoxide (O2− ) radical into ordinary oxygen (O2 ) and hydrogen peroxide (H2 O2 ), leaving the harmful superoxide anion less dangerous
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