Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Inhibitory effect of punicalagin on lipopolysaccharide-induced neuroinflammation, oxidative stress and memory impairment via inhibition of nuclear factor-kappaB

Artikel i vetenskaplig tidskrift
Författare Y. E. Kim
C. J. Hwang
H. P. Lee
C. S. Kim
D. J. Son
Y. W. Ham
Mats Hellström
S. B. Han
H. S. Kim
E. K. Park
J. T. Hong
Publicerad i Neuropharmacology
Volym 117
Sidor 21-32
ISSN 0028-3908
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, sektionen för kvinnors och barns hälsa, Avdelningen för obstetrik och gynekologi
Sidor 21-32
Språk English
Länkar doi.org/10.1016/j.neuropharm.2017.0...
Ämnesord Alzheimer's disease, Amyloidogenesis, Lipopolysaccharide, Memory impairment, Neuroinflammation, Pomegranate, Punicalagin, beta-amyloid generation, nitric-oxide synthase, in-vivo models, alzheimers-disease, pomegranate juice, b activity, protein, inflammation, expression, brain, Neurosciences & Neurology, Pharmacology & Pharmacy, geer pl, 1992, neurology, v42, p447
Ämneskategorier Klinisk medicin

Sammanfattning

Neuroinflammation is significant in the pathogenesis and development of Alzheimer's disease (AD). Previously, we showed lipopolysaccharide (LPS)-induced neuroinflammation caused memory impairment. We investigated the possible preventive effects of punicalagin (PUN), a component of pomegranate, on memory deficiency caused by LPS, along with the fundamental mechanisms. LPS-treated cultured astrocytes and microglial BV -2 cells were investigated for anti-neuroinflammatory effects of PUN. PUN (1.5 mu g/kg) ameliorates LPS (250 mu g/kg daily 7 times) -induced memory impairment as well as prevents the LPS-induced expression of inflammatory proteins. In in vitro study, we also found that PUN (1 mu g/ml) inhibited the LPS-(10, 20 and 50 mu M) induced expression of iNOS and Cox -2 as well as the production of ROS, NO, TNF-alpha and IL-1 beta(PUN also suppress activation of NF-kappa B via inhibition of I kappa B degradation as well as p50 and p65 translocation into the nucleus in LPS treated mouse brain and cultured astrocytes and microglial BV -2 cells. Consistent with the inhibitory effect on neuro inflammation, PUN inhibited LPS-induced A beta(1-42) generation through down-regulation of APP and BACE1 expression in in vivo and in vitro study. Moreover, PUN directly binds to NF-kappa B subunit p50 evidenced by a docking model and pull down assay. These results suggest that PUN inhibits LPS-induced memory impairment via anti-inflammatory and anti-amylogenic mechanisms through inhibition of NF-kappa B activation. (C) 2017 Elsevier Ltd. All rights reserved.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?