Detailed Information

Cited 52 time in webofscience Cited 55 time in scopus
Metadata Downloads

Oral Administration of Alpha Linoleic Acid Rescues A beta-Induced Glia-Mediated Neuroinflammation and Cognitive Dysfunction in C57BL/6N Miceopen access

Authors
Ali, WaqarIkram, MuhammadPark, Hyun YoungJo, Min GiUllah, RahatAhmad, SareerBin Abid, NomanKim, Myeong Ok
Issue Date
Mar-2020
Publisher
MDPI
Keywords
Alzheimer's disease; neuroinflammation; neurodegeneration; omega-3 fatty acids
Citation
CELLS, v.9, no.3
Indexed
SCIE
SCOPUS
Journal Title
CELLS
Volume
9
Number
3
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/6880
DOI
10.3390/cells9030667
ISSN
2073-4409
2073-4409
Abstract
In this work, we evaluated the effects of alpha linoleic acid (ALA), an omega-3 polyunsaturated fatty acid, on amyloid-beta-induced glial-cell-mediated neuroinflammation, amyloidogenesis, and cognitive dysfunction in mice. After an infusion of A beta(1-42) (A beta(1-42), 5 mu L/5 min/mouse, intracerebroventricular injection (i.c.v), and respective treatments of ALA (60 mg/kg per oral for six weeks), neuroinflammation, apoptotic markers, and synaptic markers were evaluated by Western blot and immunofluorescence analyses. According to our findings, the infusion of A beta(1-42) activated Toll-like receptor 4 (TLR4), glial fibrillary acidic protein (GFAP), and ionized calcium adaptor molecule 1 (Iba-1) in the frontal cortices and hippocampi of the A beta(1-42)-injected mice to a greater extent than the A beta(1-42) + ALA-cotreated mice. Similarly, there was an elevated expression of phospho-c-Jun-N-terminal kinase (p-JNK), phospho-nuclear factor-kB p65 (p-NF-kB p65 (Ser536)), and tissue necrosis factor (TNF) in the A beta(1-42) infused mouse brains; interestingly, these markers were significantly reduced in the A beta + ALA-cotreated group. The elevated expression of pro-apoptotic markers was observed during apoptotic cell death in the A beta(1-42)-treated mouse brains, whereas these markers were markedly reduced in the A beta + ALA-cotreated group. Moreover, A beta(1-42) infusion significantly increased amyloidogenesis, as assessed by the enhanced expression of the amyloid precursor proteins (APP) beta-amyloid cleaving enzyme-1 (BACE-1) and amyloid-beta (A beta(1-42)) in the mouse brains, whereas these proteins were markedly reduced in the A beta + ALA-cotreated group. We also checked the effects of ALA against A beta-triggered synaptic dysfunction and memory dysfunction, showing that ALA significantly improved memory and synaptic functions in A beta-treated mouse brains. These results indicated that ALA could be an applicable intervention in neuroinflammation, apoptotic cell loss, amyloidogenesis, and memory dysfunction via the inhibition of TLR4 and its downstream targets in A beta + ALA-cotreated mouse brains.
Files in This Item
There are no files associated with this item.
Appears in
Collections
ETC > Journal Articles

qrcode

Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.

Related Researcher

Researcher Kim, Myeong Ok photo

Kim, Myeong Ok
대학원 (응용생명과학부)
Read more

Altmetrics

Total Views & Downloads

BROWSE