Quercetin Inhibits Left Ventricular Dysfunction Induced by Chronic Stress in Rats

Tweet about this on TwitterShare on FacebookEmail this to someoneShare on Google+

Ismaeel Bin-Jaliah


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.

KEY WORDS: Quercetin; Chronic stress; Heart failure; Left ventricular dysfunction; Antioxidant; Apoptosis.

How to cite this article

BIN-JALIAH, I. Quercetin inhibits left ventricular dysfunction induced by chronic stress in rats. Int. J. Morphol., 35(2):654-660, 2017.