关键词: 阿尔茨海默病；糖基化终产物，高级；白细胞介素1；肿瘤坏死因子；小神经胶质细胞；大鼠，Wistar

Abstract:

Objective    To research the effect of advanced glycation end products (AGEs) on the levels of interleukin 1β(IL-1β) and tumor necrosis factor α(TNF-α)in primary rat microglial cells, and to further explore the effect of AGEs-BSA on Alzheimer′s disease(AD) and the possible mechanism at the cell ular level. Methods     Cultured microglial cells were intervened by AGEs-BSA and then identified with the immunocytochemistry method, and morphological changes of the cells were observed. After primary rat microglial cells were treated with 300μg/mL of AGEs-BSA and the RAGE neutralizing antibody, the levels of IL-1β and TNF-α extracted from the supernatant liquid of microglia were measured by enzyme-linked immunosobent assay(ELISA). Results     After the intervention of AGEsBSA, the cell body became bigger and the shape showed as an “Ameba”, and the levels of IL-1β and TNF-α were significantly increased（P＜0.001）. Compared with the AGEsBSA group, the levels of IL-1β and TNF-α were lower in cells exposed to the RAGE neutralizing antibody before treatment with AGEs-BSA （P＜0.01）, while they were higher than those in the normal control group（P＜0.01）. Conclusion      AGEs-BSA could activate microglia and induce the release of IL-1β and TNF-α in a time-dependent manner, which suggested that AGEs act directly or through the receptor activated microglia-mediated immune inflammatory responses.

Key words: Alzheimer disease; Glycosylation end products, advanced; Interleukin-1; Tumor necrosis factor; Microglia; Rats, Wistar