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Cited 24 time in webofscience Cited 22 time in scopus
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Anti-Amnesic Effect of Walnut via the Regulation of BBB Function and Neuro-Inflammation in A beta(1-42)-Induced Miceopen access

Authors
Kim, Jong MinLee, UkKang, Jin YongPark, Seon KyeongShin, Eun JinKim, Hyun-JinKim, Chul-WooKim, Mahn-JoHeo, Ho Jin
Issue Date
Oct-2020
Publisher
MDPI AG
Keywords
walnut; tannin; amyloid beta; cognitive dysfunction; blood– brain barrier; neuroinflammation; Akt pathway
Citation
Antioxidants, v.9, no.10, pp 1 - 24
Pages
24
Indexed
SCIE
SCOPUS
Journal Title
Antioxidants
Volume
9
Number
10
Start Page
1
End Page
24
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/6103
DOI
10.3390/antiox9100976
ISSN
2076-3921
Abstract
This study was conducted to assess the protective effect of walnut (Juglans regia L.) extract on amyloid beta (A beta)(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 A beta-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-alpha), 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-I kappa B), cyclooxygenase-2 (COX-2), and interleukin 1 beta (IL-1 beta), 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 A beta-related Akt pathway.
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