We tested a protocol with four groups: standard diet (control); high-fat diet (HF); ¦Á-tocopherol (¦Á-Toc); HF plus ¦Á-tocopherol (HF+¦Á-Toc). HF was administered ad libitum and ¦Á-Toc (50 mg/kg) by gavage. After three months of treatment we performed the behavioral tests. The biochemical assays were performed ex vivo in the cerebral cortex (CC), hippocampus (HP) and blood samples.
The behavioral tests results showed a decrease in step-down latency for the HF group (P < 0.05). When rats that received HF were treated with ¦Á-toc (HF+¦Á-Toc) the step-down latency was similar to the control group. AChE and Na+,K+-ATPase activities in homogenate and synaptosomes was observed a significant decrease in CC and HP in HF group (P < 0.05). However, ¦Á-Toc group showed to reverse the decline in AChE and Na+,K+-ATPase activities in CC and HP. HF group showed a significant increase (P < 0.05) in MDA levels in CC and HP in relation to other groups. However, ¦Á-Toc group showed a significant decrease (P < 0.05) in MDA levels when only compared with the HF group. Blood AChE activity increased in ¦Á-Toc group (P < 0.05) and decreased in HF group (P < 0.05) compared to all groups.
The present outcomes showed that treatment with ¦Á-Toc prevents the inhibition of AChE and Na+,K+-ATPase activities and consequently memory impairment induced by HF diet, demonstrating that this compound can modulate cholinergic neurotransmission and consequently improve cognition in this experimental condition.