The effects of apoptosis vulnerability markers on the myocardium in depression after myocardial infarction

Abstract

BackgroundThere 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.MethodsRats 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.ResultsIn 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.ConclusionsThese 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.

Quercetin Inhibits Chronic Stress-Induced Myocardial Infarction in Rats

“…It is in agreement with previous reports where mild type of CUS in rats induced the proapoptotic Bax protein in the myocardium (Dang et al, 2016), caused myocardial injury and increased cardiomyocyte apoptosis in cultured cells. Also, it is in agreement with the report that showed stress-induced overproduction of oxidative stress biomarkers caused apoptosis and enhanced levels of lipid peroxidation and peroxynitrite that damages DNA in heart tissues (Wang et al, 2013).…”

Cardiac stem cell transplantation with 2,3,5,4′-tetrahydroxystilbehe-2-O-β-d-glucoside improves cardiac function in rat myocardial infarction model

“…Finally, the sections were counterstained with hematoxylin. For negative control experiments, primary antibodies were omitted [31].…”

“…Surgical procedures were performed using a well-established technique [30,31]. Rats were anesthetized with 10% chloral hydrate (0.3 mL/100 g), intubated, and maintained on a ventilator (60 respirations/min).…”

Role of Continuous High Thoracic Epidural Anesthesia in Hippocampal Apoptosis after Global Cerebral Ischemia in Rats

“…The Bax/Bcl-2 ratio is a measure of a cell's vulnerability to apoptosis, and the ratio may be more important than either promoter alone in determining apoptosis [46]. In the downstream mitochondrial pathway of apoptosis, activated caspase-3, recognizing the structure of PARP, generates two proteolytic products: a 29 kD and a 89 kD fragments [47], which is considered a hallmark of apoptosis [5].…”