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[β-amyloid protein up-regulates the expression of the receptor for advanced glycation end products by increasing ROS production].

OBJECTIVE
To investigate the mechanism of β-amyloid protein (Aβ) in regulating the expression of the receptor for advanced glycation end products (RAGE).


METHODS
Aβ1-40 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.


RESULTS
Injection 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.


CONCLUSION
Aβ up-regulates the expression of RAGE in rat hippocampus via NADPH/ ROS/NF-κB signaling pathway.