Pelargonidin exhibits restoring effects against amyloid β-induced deficits in the hippocampus of male rats

Abstract

Background: Alzheimer's disease (AD) is characterized by amyloid-beta plaques, neuronal loss, and cognitive dysfunction. Oxidative stress plays a key role in the pathophysiology of AD, and it has been suggested that antioxidants may slow the progress of the disease. In this study, the possible protective effects of pelargonidin (a natural flavonoid) against amyloid β (Aβ)-induced behavioral deficits was investigated in rats. Methods: Adult Wistar male rats were treated with intrahippocampal injections of the Aβ (aa 25-35) and intraperitoneal injection of pelargonidin. Learning and spatial memory were tested using the Morris water maze (MWM) task. The antioxidant activity was evaluated using the ferric reducing/antioxidant power assay (FRAP assay). Data were analyzed using SPSS 20, and value of p≤0.05 was considered significant. Results: The results of this study showed that Aβ significantly increased escape latency and the distance traveled in the MWM, and pelargonidin attenuated these behavioral changes. Aβ induced a significant decrease in the total thiol content of hippocampus, and pelargonidin restored the hippocampal antioxidant capacity. Conclusion: The results of this study suggest that pelargonidin can improve Aβ-induced behavioral changes in rats.

Cotinine and 6-Hydroxy-L-Nicotine Reverses Memory Deficits and Reduces Oxidative Stress in Aβ25-35-Induced Rat Model of Alzheimer’s Disease

“…This fragment retains most of the physical and biological properties of its parent molecule, including toxicity to neurons [80,81]. The brain injection of Aβ 25-35 peptide was reported to induce behavioral changes, especially in terms of memory, in rodents, and can be used to induce an animal model of AD [41,82,83].…”

“…The ROS production can be catalyzed by redox-active metal ions when they are bounded to Aβ [99]. Aβ 25-35 caused oxidative stress in different animal cell cultures [100,101] and rat hippocampus [82]. We further evaluated the effects of nicotinic derivatives on oxidative stress in the Aβ 25-35 peptide-induced rat model of AD by measuring the SOD, CAT and GPX specific activities and the levels of GSH, MDA and carbonylated proteins in rat hippocampus.…”