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

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. Twenty-eight male adult rats were divided into sham, AD, AD+PG (5 μg, intracerebroventricular), and PG (5 μg, intracerebroventricular) groups. Intracerebroventricular (ICV) injection of Aβ peptides (6 μg) was done using stereotaxic surgery. ICV administration of PG or saline was performed daily for 28 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. The ICV injection of Aβ reduced step-through latency and discrimination index in behavioral tests (p<0.001). Aβ increased the number of apoptotic neurons (p<0.001). PG treatment decreased the time spent in the dark compartment and neuronal apoptosis in the AD+PG rats (p<0.001). PG increased the discrimination index in the NOR test (p<0.001). Although PG did not change behavioral variables, it decreased cell death in the PG group. 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.

Déclaration de conflit d'intérêts

The authors have declared that there is no conflict of interest.