Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-β25–35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by dementia and the aggregation of the amyloid beta peptide (Aβ). Aβ25–35 is the most neurotoxic sequence, whose mechanism is associated with the neuronal death in the Cornu Ammonis 1 (CA1) region of the hippocampus (Hp) and cognitive damage. Likewise, there are mechanisms of neuronal survival regulated by heat shock proteins (HSPs). Studies indicate that pharmacological treatment with flavonoids reduces the prevalence of AD, particularly epicatechin (EC), which shows better antioxidant activity. The aim of this work was to evaluate the effect of EC on neurotoxicity that causes Aβ25–35 at the level of spatial memory as well as the relationship with immunoreactivity of HSPs in the CA1 region of the Hp of rats. Our results show that EC treatment reduces the deterioration of spatial memory induced by the Aβ25–35, in addition to reducing oxidative stress and inflammation in the Hp of the animals treated with EC + Aβ25–35. Likewise, the immunoreactivity to HSP-60, -70, and -90 is lower in the EC + Aβ25–35 group compared to the Aβ25–35 group, which coincides with a decrease of dead neurons in the CA1 region of the Hp. Our results suggest that EC reduces the neurotoxicity induced by Aβ25–35, as well as the HSP-60, -70, and -90 immunoreactivity and neuronal death in the CA1 region of the Hp of rats injected with Aβ25–35, which favors an improvement in the function of spatial memory.

Keywords

• reactive oxygen species
• proinflammatory cytokines
• Alzheimer’s disease