Protective effect of chronic administration of pelargonidin on neuronal apoptosis and memory process in amyloid-beta-treated rats

Objective: Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with impaired cognitive skills and learning and memory dysfunctions.  It has been suggested that pelargonidin (PG), as an antioxidant agent, has a neuroprotective effect. PG could prevent damaging effects of amyloid-beta (Aβ) deposition. The aim of this study was to determine the chronic effect of PG on hippocampal neurons and memory processes in a rat model of AD. Materials and Methods: Twenty-eight male adult rats were divided into sham, AD, AD+PG (۵ μg, intracerebroventricular), and PG (۵ μg, intracerebroventricular) groups. Intracerebroventricular (ICV) injection of Aβ peptides (۶ μg) was done using stereotaxic surgery. ICV administration of PG or saline was performed daily for ۲۸ consecutive days. Behavioral analysis was performed using the novel object recognition (NOR) and passive avoidance tests. Neuronal apoptosis was detected using TUNEL assay in the hippocampus. Results: The ICV injection of Aβ reduced step-through latency and discrimination index in behavioral tests (p <۰.۰۰۱). Aβ increased the number of apoptotic neurons (p <۰.۰۰۱). PG treatment decreased the time spent in the dark compartment and neuronal apoptosis in the AD+PG rats (p <۰.۰۰۱). PG increased the discrimination index in the NOR test (p <۰.۰۰۱).  Although PG did not change behavioral variables, it decreased cell death in the PG group. Conclusion: PG attenuated neuronal apoptosis and improved cognition and memory deficiency in AD rats. The protective effect of PG against Aβ may be due to its anti-apoptotic property. It is suggested that PG can be useful to treat AD.

کلیدواژه ها:

Alzheimer’s disease ، Hippocampus ، Learning and memory ، Pelargonidin ، Apoptosis