The effects of apoptosis vulnerability markers on the myocardium in depression after myocardial infarction
- Equal contributors
1 Department of Psychiatry, Hospital Affiliated to Guiyang Medical University, 28 Guiyi Street, Guiyang City, 550004, Guizhou, China
2 School of Medicine, Deakin University, 1 Gheringhap Street, Geelong, VIC 3220, Australia
3 Department of Cardiology, Hospital Affiliated to Guiyang Medical University, 28 Guiyi Street, Guiyang City, 550004, Guizhou, China
4 Department of Neurology, The General Hospital of Hebi Coal Corp, 84 Honggi Street, Hebi City, 458000, Henan, China
5 Department of Psychiatry, The University of Melbourne, Level 1, North Block Main, Building Royal Melbourne Hospital, Parkville, VIC 3050, Australia
6 Orygen Youth Health Research Centre, Centre for Youth Mental Health, 35 Poplar, Road, Parkville VIC 3052, Australia
7 Florey Institute of Neuroscience and Mental Health, Level 3, Alan Gilbert Building, 161 Barry Street, University of Melbourne, Parkville, VIC 3010, Australia
BMC Medicine 2013, 11:32 doi:10.1186/1741-7015-11-32Published: 8 February 2013
There is an increased incidence of major depressive disorder (MDD) in individuals after myocardial infarction (MI), but the pathophysiological processes mediating this association are unclear. Our previous study demonstrated an increase in pro-apoptotic pathways in the myocardium and hippocampus in MDD, which was reversed by venlafaxine. This study aimed to attempt to confirm the effects of apoptosis vulnerability markers on the myocardium in a model of depression after myocardial infarction.
Rats were divided into four groups: sham (N = 8), depression (N = 8, chronic mild unpredictable stress and separation were used in the depression group), MI (N = 13) and post-MI depression (N = 7). The rats in all four groups underwent the same open field and sucrose preference behavioral tests. Evan Blue staining was used to determine the area at risk of myocardial infarction in the left ventricle, and 2,3,5-triphenyl tetrazolium chloride (1.5% TTC) dye was used to detect the size of the myocardial infarction. The expression of bax and bcl-2 protein in the myocardium was investigated by immunohistochemistry, and the mRNA expression of bax, bcl-2 and caspase-3 in the myocardium was investigated by real time RT-PCR. Apoptosis was estimated in the myocardium by measuring the Bax:Bcl-2 ratio.
In the depression and post-MI depression rats, there were significantly decreased movements and total sucrose consumption, modeling behavioral deficits and an anhedonic-like state. In terms of myocardial infarction size, no difference was seen between the MI and post-MI depression groups. There was an up-regulated Bax:Bcl-2 ratio in the depression, MI and post-MI depression groups. Furthermore, in the latter group, there was a greater up-regulated Bax:Bcl-2 ratio. However, caspase-3 did not differ among the four groups.
These results of this animal model suggest that active pro-apoptotic pathways may be involved in the nexus between myocardial infarction and depression. This mechanism may be germane to understanding this relationship in humans.