Abstract
Post-MI depression is a critical clinical problem, the comorbidity of which complicates depression treatment and worsens cardiovascular outcomes. However, which antidepressant is the best to lower the risk of cardiovascular events in persons with depression was still unknown. Recently, it has been proposed that the activation of ALDH2 by Alda-1 can effectively reduce depressive-like behaviors and improve the prognosis of coronary heart disease. In the present study, we investigated the effect of Alda-1 on the expression of VEGF in the hippocampus of a rat model with post-MI depression, as well as the potential treatment mechanism. Alda-1 administration significantly decreased the immobility time and increased the swimming time of the post-MI depression rats in the forced swim test. Moreover, treatment of post-MI depression rats with Alda-1 significantly increased the sucrose preference ratio, as assessed by a sucrose preference test. These behaviors were associated with an increase 5-HT and DA neurotransmitter content, as well as an increase of VEGF levels in the hippocampus of the post-MI depression rats. These results suggest that Alda-1 improves depressive-like behavior in rats after MI by increasing VEGF expression in the hippocampus of rats.