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Neuroprotective effects of paeoniflorin against neuronal oxidative stress and neuroinflammation induced by lipopolysaccharide in miceopen access

Authors
Meng, H.W.Lee, A.Y.Kim, H.Y.Cho, E.J.Kim, J.H.
Issue Date
Mar-2022
Publisher
Korean Society for Applied Biological Chemistry
Keywords
Alzheimer’s disease; Lipopolysaccharide; Neuroinflammation; Oxidative stress; Paeoniflorin
Citation
Journal of Applied Biological Chemistry, v.65, no.1, pp 23 - 31
Pages
9
Indexed
SCOPUS
KCI
Journal Title
Journal of Applied Biological Chemistry
Volume
65
Number
1
Start Page
23
End Page
31
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/2673
DOI
10.3839/jabc.2022.004
ISSN
1976-0442
2234-7941
Abstract
Oxidative stress and neuroinflammation play important roles in the pathogenesis of Alzheimer's disease (AD). This study investigated the protective effects of paeoniflorin (PF) against neuronal oxidative stress and neuroinflammation in lipopolysaccharide (LPS)-induced mice. The brains of LPS-injected control group showed significantly increased neuroinflammation by activating the nuclear factor kappa B (NF-κB) pathway and increasing inflammatory mediators. However, administration of PF significantly attenuated oxidative stress by inhibiting lipid peroxidation, nitric oxide levels, and reactive oxygen species production in the brain; PF at doses of 5 and 10 mg/kg/day downregulated the expression of NF-κB pathway-related proteins and significantly decreased inflammatory mediators including inducible nitric oxide synthase and cyclooxygenase-2. Moreover, the levels of brain-derived neurotrophic factor and its receptor, tropomycin receptor kinase B, were significantly increased in PFtreated mice. Furthermore, acetylcholinesterase activity and the ration of B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X were significantly reduced by PF in the brains of LPS-induced mice, resulting in the inhibition of cholinergic dysfunction and neuronal apoptosis. Thus, we can conclude that administration of PF to mice prevents the development of LPS-induced AD pathology through the inhibition of neuronal oxidative stress and neuroinflammation, suggesting that PF has a therapeutic potential for AD. ? The Korean Society for Applied Biological Chemistry 2022.
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