A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.

Depression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredi...

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Main Authors: Wang Xinxing, Liu Wei, Wu Lei, Zhan Rui, Jin Baoying, Qian Lingjia
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3923793?pdf=render
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spelling doaj-69307bfaca9b42e39e33a5b23c48210d2020-11-25T01:23:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8842710.1371/journal.pone.0088427A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.Wang XinxingLiu WeiWu LeiZhan RuiJin BaoyingQian LingjiaDepression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredictable mild stress (CUMS) on myocardial injury and to further elucidate the biological mechanism of depression. Rats were used as a model. The CUMS procedure lasted for a total of 8 weeks. After 4 weeks of CUMS, treated rats exhibited a reduced sucrose preference and changes in scores on an open field test, body weight and content of 5-HT in the brain as compared with the values of these variables in controls. These changes indicated depression-like changes in CUMS rats and demonstrated the feasibility of the depression model. In addition, pathological changes in the myocardium and increased cardiomyocyte apoptosis demonstrated that myocardial injury had occurred after 6 weeks of CUMS and had increased significantly by the end of 8 weeks of CUMS. Plasma serotonin (5-HT), norepinephrine (NE) and epinephrine (E), all depression-related neuroendocrine factors, were measured by HPLC-ECD techniques, and the content of plasma corticosterone (GC) was evaluated by an I(125)-cortisol radioactivity immunoassay in control and CUMS rats. The results indicated that 5-HT had decreased, whereas NE, E and GC had increased in CUMS rats, and these factors might be associated with depression-induced myocardial injury. The effects of 5-HT, NE and GC on the survival rate of cultured cardiomyocytes were determined using an orthogonal design. The results showed that 5-HT was a more important factor affecting cell survival than GC or NE. The results suggested that normal blood levels of 5-HT had a cytoprotective effect. The neuroendocrine disorders characterized by decreased 5-HT combined with increased GC and NE mediated the occurrence of depression-induced myocardial injury.http://europepmc.org/articles/PMC3923793?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Wang Xinxing
Liu Wei
Wu Lei
Zhan Rui
Jin Baoying
Qian Lingjia
spellingShingle Wang Xinxing
Liu Wei
Wu Lei
Zhan Rui
Jin Baoying
Qian Lingjia
A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
PLoS ONE
author_facet Wang Xinxing
Liu Wei
Wu Lei
Zhan Rui
Jin Baoying
Qian Lingjia
author_sort Wang Xinxing
title A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
title_short A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
title_full A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
title_fullStr A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
title_full_unstemmed A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
title_sort neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2014-01-01
description Depression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredictable mild stress (CUMS) on myocardial injury and to further elucidate the biological mechanism of depression. Rats were used as a model. The CUMS procedure lasted for a total of 8 weeks. After 4 weeks of CUMS, treated rats exhibited a reduced sucrose preference and changes in scores on an open field test, body weight and content of 5-HT in the brain as compared with the values of these variables in controls. These changes indicated depression-like changes in CUMS rats and demonstrated the feasibility of the depression model. In addition, pathological changes in the myocardium and increased cardiomyocyte apoptosis demonstrated that myocardial injury had occurred after 6 weeks of CUMS and had increased significantly by the end of 8 weeks of CUMS. Plasma serotonin (5-HT), norepinephrine (NE) and epinephrine (E), all depression-related neuroendocrine factors, were measured by HPLC-ECD techniques, and the content of plasma corticosterone (GC) was evaluated by an I(125)-cortisol radioactivity immunoassay in control and CUMS rats. The results indicated that 5-HT had decreased, whereas NE, E and GC had increased in CUMS rats, and these factors might be associated with depression-induced myocardial injury. The effects of 5-HT, NE and GC on the survival rate of cultured cardiomyocytes were determined using an orthogonal design. The results showed that 5-HT was a more important factor affecting cell survival than GC or NE. The results suggested that normal blood levels of 5-HT had a cytoprotective effect. The neuroendocrine disorders characterized by decreased 5-HT combined with increased GC and NE mediated the occurrence of depression-induced myocardial injury.
url http://europepmc.org/articles/PMC3923793?pdf=render
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