The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression

BMC Psychiatry

Michael Berk¹  Xingde Liu²  Fangxian Chai⁴  Hongming Zhang³  Yiming Wang⁴ 

[1] Florey Institute of Neuroscience and Mental Health, University of Melbourne, Level 3, Alan Gilbert Building, Parkville 3010, VIC, Australia;Department of Cardiology, Hospital Affiliated to Medical University, 28 Guiyi Street, Guiyang City 550004, Guizhou, China;Department of Cardiology, The General Hospital of Jinan Military Region, Jinan 250031, China;Department of Psychiatry, Hospital Affiliated to Guiyang Medical University, Guiyang 550004, Guizhou, China

关键词: Bcl-2;    Bax;    Myocardial infarction;    Depression;    Escitalopram;   

Others  :  1091549
DOI  :  10.1186/s12888-014-0349-x

 received in 2014-05-08, accepted in 2014-11-24,  发布年份 2014

【 摘 要 】

Background

Major depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R).

Methods

Rats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat’s left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl–2 and Bax.

Results

Compared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P < .01). Compared with the DI/R group, the myocardial infarct size in the escitalopram + DI/R group was significantly decreased (P < .01). Compared with the D group, there were significantly increased apoptotic myocardial cells in the DI/R and escitalopram + DI/R groups (P < .01); however compared with the DI/R group, apoptotic myocardial cell numbers in the escitalopram + DI/R group were significantly decreased (P < .01). Compared with the DI/R group, there was a down-regulated Bax:Bcl-2 ratio in the escitalopram + DI/R group (P < .01).

Conclusions

These results suggest that in patients with AMI comorbid with MDD, there is an increase in pro-apoptotic pathways that is reversed by escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction.

【 授权许可】

   
2014 Wang et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

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