β-amyloid protein up-regulates the expression of the receptor for advanced glycation end products by increasing ROS production.
- Author:
Weina KONG
1
;
Jia ZHANG
;
Weijuan GAO
;
Qingtao LIU
;
Liming ZHOU
;
Xiqing CHAI
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; adverse effects; Animals; Hippocampus; metabolism; Male; Membrane Glycoproteins; metabolism; NADP; metabolism; NADPH Oxidase 2; NADPH Oxidases; metabolism; NF-kappa B; metabolism; Oxidative Stress; Peptide Fragments; adverse effects; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; metabolism; Receptor for Advanced Glycation End Products; Receptors, Immunologic; metabolism; Signal Transduction; Up-Regulation
- From: Journal of Southern Medical University 2013;33(8):1132-1136
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of β-amyloid protein (Aβ) in regulating the expression of the receptor for advanced glycation end products (RAGE).
METHODSAβ1-40 was injected into the bilateral hippocampus of rats, and 3 weeks later, the levels of reactive oxygen species (ROS) production were detected by flow cytometry. The expressions of RAGE, reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (gp9l(phox) and p47(phox)), nuclear factor-κB (NF-κB), and inhibitor of κB (IκB) were measured by Western blotting.
RESULTSInjection of Aβ1-40 caused a significant increase in the expressions of RAGE, gp9l(phox), p47(phox), phospho-p47(phox), phospho-IκBα, NF-κB and phospho-NF-κB in rat hippocampus but decreased the level of IκBα. Aβ1-40 injection also resulted in a significantly increased content of ROS in the hippocampus of the rats.
CONCLUSIONAβ up-regulates the expression of RAGE in rat hippocampus via NADPH/ ROS/NF-κB signaling pathway.
