Abstract:

Objective   To investigate effects of advanced glycation end products (AGEs) on the cell morphology， survival rate, apoptosis rate, choline acetyltransfesterase (ChAT) activity and acetylcholine(AchE) activity of the cultured primary rat basal forebrain cholinergic neurons. To explore the effect and the possible mechanism of AGEs in Alzheimer′s disease(AD) at the cell level. Methods   Cultured primary rat basal forebrain cholinergic neurons were intervened by AGE-BSA and the RAGE neutralizing antibody， then the cell morphological changes were observed and detected by the immunofluorescence method and the inverted microscope. Cell survival rates were determined by MTT. Cells apoptosis rate was measured by flow cytometry and the activities of ChAT and AchE were measured by colorimetry. Results   After 72 hours, injury changes of the morphology took place in the neurons, the survival rates and apoptosis rates were higher, the ChAT activity significantly reduced, and the AchE activity significantly increased compared with the control group. The survival rates and ChAT activity of the AGE-BSA+anti-RAGE group also reduced， and the apoptosis rates and AchE activity increased, but the changes of AGEBSA+antiRAGE group was lower than the AGE-BSA group. Conclusion   AGE-BSA can cause the apoptosis of the primary rat basal forebrain cholinergic neurons after 72 hours， lead to the reduction of the ChAT activity and increase the AchE activity. The blocking combination of AGE-BSA and its receptor RAGE can reduce the injury effects, which suggests that advanced glycation end products may activate the injury effects on the cholinergic neurons through the receptor RAGE.

Key words: Alzheimer′s disease; Advanced glycation end products; Cholinergic  neurons; Choline acetyltransfesterase； Acetylcholine； Rat, Wistar