The effect of meloxicam on the inflammatory reaction induced by beta amyloid protein in Alzheimer's disease rats.
- Author:
Jia-hui MAO
1
;
Ai-ling ZHOU
;
Ya-e HU
;
Yan ZHU
;
Hai-yan SHI
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; chemically induced; drug therapy; pathology; Amyloid beta-Peptides; toxicity; Animals; Cerebral Cortex; metabolism; pathology; Glial Fibrillary Acidic Protein; metabolism; Inflammation; prevention & control; Interleukin-1beta; metabolism; Male; Peptide Fragments; toxicity; Rats; Rats, Sprague-Dawley; Thiazines; pharmacology; therapeutic use; Thiazoles; pharmacology; therapeutic use; Transcription Factor RelA; metabolism; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Applied Physiology 2010;26(1):66-70
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect and mechanism of meloxicam on the inflammatory reaction induced by beta amyloid protein (AB) in Alzheimer's disease (AD) rats.
METHODSThe rat model was established by microinjection of Abeta(1-40) into hippocampus. The expression of NF-kappaB p65 and glial fibrillary acidic protein (GFAP) in hippocampus were detected by immunohistochemistry. The content of GFAP in cortex was tested by Western-blot. The content of TNF-alpha in cortex was tested by ELISA. The expression of IL-1beta mRNA was tested by RT-PCR.
RESULTSThe expression of NF-kappaB p65, GFAP and TNF-alpha as well as IL-1beta mRNA were decreased by meloxicam.
CONCLUSIONMeloxicam can reduce the proliferation of astrocyte by decreasing the expression of GFAP in AD model rat's hippocampus and cortex. And the depression of NF-kappaB p65 may significantly decrease the expression of TNF-alpha1 and IL-1beta to lessen the inflammatory reaction in cerebral tissue.
