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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

Wang,Y, Zhang,H, Chai,F, Liu,X and Berk,M 2014, 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, vol. 14, no. 1, pp. 1-7, doi: 10.1186/s12888-014-0349-x.

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Title 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
Author(s) Wang,Y
Zhang,H
Chai,F
Liu,X
Berk,MORCID iD for Berk,M orcid.org/0000-0002-5554-6946
Journal name BMC Psychiatry
Volume number 14
Issue number 1
Start page 1
End page 7
Publisher BioMed Central
Place of publication London, England
Publication date 2014-12-04
ISSN 1471-244X
Keyword(s) Science & Technology
Life Sciences & Biomedicine
Psychiatry
Escitalopram
Depression
Myocardial infarction
Bax
Bcl-2
ISCHEMIA-REPERFUSION INJURY
UNPREDICTABLE MILD STRESS
CORONARY-HEART-DISEASE
SERTRALINE TREATMENT
INDUCED ANHEDONIA
CELL-DEATH
INFARCTION
MORTALITY
ANTIDEPRESSANT
METAANALYSIS
Summary BackgroundMajor 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).MethodsRats 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.ResultsCompared 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).ConclusionsThese 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.
Language eng
DOI 10.1186/s12888-014-0349-x
Field of Research 110319 Psychiatry (incl Psychotherapy)
Socio Economic Objective 920410 Mental Health
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, BioMed Central
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30068827

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Open Access Collection
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.