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
| Autor: | Hongming Zhang, Yiming Wang, Michael Berk, Fangxian Chai, Xingde Liu |
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| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Infarction Apoptosis Myocardial Reperfusion Injury Citalopram Rats Sprague-Dawley 03 medical and health sciences Escitalopram 0302 clinical medicine Bcl-2-associated X protein Internal medicine mental disorders medicine Animals Humans Bcl-2 Myocardial infarction bcl-2-Associated X Protein 030304 developmental biology Depressive Disorder Major 0303 health sciences TUNEL assay biology Depression business.industry Myocardium medicine.disease Pathophysiology Rats 3. Good health Disease Models Animal Psychiatry and Mental health Treatment Outcome Endocrinology Proto-Oncogene Proteins c-bcl-2 Bax Anesthesia biology.protein Antidepressant business 030217 neurology & neurosurgery Research Article medicine.drug |
| Zdroj: | BMC Psychiatry |
| ISSN: | 1471-244X |
| DOI: | 10.1186/s12888-014-0349-x |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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