摘要

The present study aimed to investigate the effects of intestinal endotoxemia (IETM) in a rat model of aluminum neurotoxicity established by D-galactose and aluminum trichloride (AlCl3). Adult Wistar rats were administered D-galactose and AlCl3 to create the aluminum neurotoxicity model. The learning and memory abilities of the rats were subsequently observed using a Morris water maze test and the serum levels of lipopolysaccharide (LPS), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, diamine oxidase (DAO), glutamine (Gln) and glutaminase were measured. The expression of S-100 beta in the serum was detected using an enzyme-linked immunosorbent assay. The expression levels of the amyloid beta-protein (A beta) precursor (APP), presenilin 1 (PS1), beta-site APP-cleaving enzyme (BACE), zona occludens protein (ZO)-1 and A beta 1-40 in the brain of rats were detected via reverse-transcription polymerase chain reaction, western blotting and immunohistochemistry. The levels of LPS, TNF-alpha, IL-1, DAO, Gln and S-100 beta in serum and the mRNA and protein expression levels of APP, PS1, BACE and A beta 1-40 in the brain were markedly increased in the model rats compared with controls. The level of glutaminase in the serum and the expression of ZO-1 in the brain were decreased in the model rats compared with controls. IETM was present in the rat model of aluminum neurotoxicity established by D-galactose and AlCl3 and may be important in the development of this neurotoxicity.