Abstract
This study was conducted to assess the protective effect of walnut (Juglans regia L.) extract on amyloid beta (Aβ)1-42-induced institute of cancer research (ICR) mice. By conducting a Y-maze, passive avoidance, and Morris water maze tests with amyloidogenic mice, it was found that walnut extract ameliorated behavioral dysfunction and memory deficit. The walnut extract showed a protective effect on the antioxidant system and cholinergic system by regulating malondialdehyde (MDA) levels, superoxide dismutase (SOD) contents, reduced glutathione (GSH) contents, acetylcholine (ACh) levels, acetylcholinesterase (AChE) activity, and protein expression of AChE and choline acetyltransferase (ChAT). Furthermore, the walnut extract suppressed Aβ-induced abnormality of mitochondrial function by ameliorating reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and ATP contents. Finally, the walnut extract regulated the expression of zonula occludens-1 (ZO-1) and occludin concerned with blood–brain barrier (BBB) function, expression of tumor necrosis factor-alpha (TNF-α), tumor necrosis factor receptor 1 (TNFR1), phosphorylated c-Jun N-terminal kinase (p-JNK), phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (p-IκB), cyclooxygenase-2 (COX-2), and interleukin 1 beta (IL-1β), related to neuroinflammation and the expression of phosphorylated protein kinase B (p-Akt), caspase-3, hyperphosphorylation of tau (p-tau), and heme oxygenase-1 (HO-1), associated with the Aβ-related Akt pathway.
Highlights
Alzheimer’s disease (AD) is caused by cerebral neurodegeneration and is accompanied by memory loss and cognitive dysfunction in elders [1]
AD is a degenerative disease caused by inflammatory responses and oxidative stress in the system
AD neuronal is a degenerative by inflammatory responses and oxidative stress in the induced by the aggregation of Aβ [30]
Summary
Alzheimer’s disease (AD) is caused by cerebral neurodegeneration and is accompanied by memory loss and cognitive dysfunction in elders [1]. The mechanism of neurodegeneration of AD is unknown, excessive oxidative stress and inflammatory toxicity derived from amyloid beta (Aβ) are considered to be among the main causes of AD [2]. In the amyloid metabolism pathway, Aβ produced by beta-secretase (BACE) and γ- secretase aggregates within the cell [3]. Aβ peptides are commonly found in the brain in the form of Aβ1-40 and Aβ1–42 , and in particular, Aβ1-42 are more toxic than other species. Aβ1-42 is deposited in senile plaques and capillaries, resulting in greater toxicity [4]. The agglutination of Aβ1–42 causes the activation of inflammatory responses, production of oxidative
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