Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats

Complications of chronic stress including cardiovascular disease are among the common public health problems that affect the lives of millions of people around the globe. We sought to determine whether the anti-oxidant and anti-apoptotic agent, quercetin can inhibit chronic stress-induced left ventr...

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Autor principal: Bin-Jaliah,Ismaeel
Lenguaje:English
Publicado: Sociedad Chilena de Anatomía 2017
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000200044
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spelling oai:scielo:S0717-950220170002000442017-08-07Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in RatsBin-Jaliah,Ismaeel Quercetin Chronic stress Heart failure Left ventricular dysfunction Antioxidant Apoptosis Complications of chronic stress including cardiovascular disease are among the common public health problems that affect the lives of millions of people around the globe. We sought to determine whether the anti-oxidant and anti-apoptotic agent, quercetin can inhibit chronic stress-induced left ventricular dysfunction (LVD). Chronic unpredictable stress (CUS) was induced in rats using a variety of stressors in the presence and absence of quercetin (50 mg/kg body weight/day). Harvested tissues from the left ventricles (LV) of these animals were examined using basic histological staining. In addition, LV tissue homogenates were assayed for markers of oxidative and anti-oxidative stress that are known to be modulated in cardiac dysfunction. Furthermore, LV pressure was monitored by a pressure catheter inserted directly into the LV. Histopathological examinations of the LV in the model group (CUS) showed a profound damage to LV compared to the control group as demonstrated by a severe damage of cardiomyocytes and an increase of inflammatory cell infiltration, which was prevented by quercetin. CUS increased LV end-diastolic pressure that was significantly blocked by quercetin. In addition, quercetin significantly (p<0.05) blocked CUS-induced inhibition of the anti-oxidant superoxide dismutase (SOD) and the survival Bcl-2 proteins. Quercetin also significantly (p<0.05) inhibited CUS-induced augmentation of the oxidative stress TBARS and the apoptotic protein caspase-3. We conclude that LVD induced by CUS possibly via activation of oxidative and apoptosis pathways can be inhibited by quercetin; thus may offer therapeutic potential in humans.info:eu-repo/semantics/openAccessSociedad Chilena de AnatomíaInternational Journal of Morphology v.35 n.2 20172017-06-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000200044en10.4067/S0717-95022017000200044
institution Scielo Chile
collection Scielo Chile
language English
topic Quercetin
Chronic stress
Heart failure
Left ventricular dysfunction
Antioxidant
Apoptosis
spellingShingle Quercetin
Chronic stress
Heart failure
Left ventricular dysfunction
Antioxidant
Apoptosis
Bin-Jaliah,Ismaeel
Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
description Complications of chronic stress including cardiovascular disease are among the common public health problems that affect the lives of millions of people around the globe. We sought to determine whether the anti-oxidant and anti-apoptotic agent, quercetin can inhibit chronic stress-induced left ventricular dysfunction (LVD). Chronic unpredictable stress (CUS) was induced in rats using a variety of stressors in the presence and absence of quercetin (50 mg/kg body weight/day). Harvested tissues from the left ventricles (LV) of these animals were examined using basic histological staining. In addition, LV tissue homogenates were assayed for markers of oxidative and anti-oxidative stress that are known to be modulated in cardiac dysfunction. Furthermore, LV pressure was monitored by a pressure catheter inserted directly into the LV. Histopathological examinations of the LV in the model group (CUS) showed a profound damage to LV compared to the control group as demonstrated by a severe damage of cardiomyocytes and an increase of inflammatory cell infiltration, which was prevented by quercetin. CUS increased LV end-diastolic pressure that was significantly blocked by quercetin. In addition, quercetin significantly (p<0.05) blocked CUS-induced inhibition of the anti-oxidant superoxide dismutase (SOD) and the survival Bcl-2 proteins. Quercetin also significantly (p<0.05) inhibited CUS-induced augmentation of the oxidative stress TBARS and the apoptotic protein caspase-3. We conclude that LVD induced by CUS possibly via activation of oxidative and apoptosis pathways can be inhibited by quercetin; thus may offer therapeutic potential in humans.
author Bin-Jaliah,Ismaeel
author_facet Bin-Jaliah,Ismaeel
author_sort Bin-Jaliah,Ismaeel
title Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
title_short Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
title_full Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
title_fullStr Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
title_full_unstemmed Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats
title_sort quercetin inhibits left ventricular dysfunction induced by chronic stress in rats
publisher Sociedad Chilena de Anatomía
publishDate 2017
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0717-95022017000200044
work_keys_str_mv AT binjaliahismaeel quercetininhibitsleftventriculardysfunctioninducedbychronicstressinrats
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