Effects of Sigma-1 receptor on atrial arrhythmia in depression rat models

Abstract

Objective To assess the effect of Sigma-1 receptor on atrial arrhythmia in depression rats, we provide clinical potential therapeutic targets of depression with atrial fibrillation. Methods Fifty-five male SD rats were randomly divided into 3 groups: control group (CTL group, n=15), depression group (D group, n=20), and depression with Sigma-1 agonist group (Sigma-1 group, n=20). Depression model was set up by chronic unpredictable mild stress.Sucrose preference test, forced swimming test and body weight test were performed to define the completion of the model.DSI was implanted to detect the incidence of atrial arrhythmia.Masson staining to assess myocardial fibrosis.And Western blot to show the expression of Sigma-1 receptor in atrium and hippocampus. Results ①The results of sucrose preference test, forced swimming test and body weight test displayed that the model was successful.②Compared to the CTL, the heart rate was significantly accelerated by depression [(517.60±19.12) min vs.(372.40±19.38) min, P<0.01]. There was no statistical difference between the Sigma-1 group and CTL group.Depression significantly increased the incidence of atrial fibrillation [9.73±2.14 vs.0, P<0.01]. ③Compared to the CTL group, the depression significantly increased myocardial fibrosis [(9.88±0.66) % vs.(1.60±0.34) %, P<0.01]. Nevertheless Sigma-1 agonists significantly reduced the degree of fibrosis[(2.12±0.72) % vs.(1.60±0.34) %, P<0.01]. ④Compared with CTL group, the expression of Sigma-1 receptor significantly decreased in atrial myocardium and hippocampus (P<0.05). The Sigma-1 agonists could significantly improve the decline of the expression in the atrium. Conclusion The over expression of Sigma-1 receptor in atrial myocytes may be one of the molecular mechanisms for reducing atrial arrhythmias in depression rat models. Key words: Depression; Atrial arrhythmia; Sigma-1 receptor