Quercetin improves postischemic recovery of heart function in doxorubicin-treated rats and prevents doxorubicin-induced matrix metalloproteinase-2 activation and apoptosis induction.

Quercetin (QCT) is flavonoid that possesses various biological functions including anti-oxidative and radical-scavenging activities. Moreover, QCT exerts some preventive actions in treatment of cardiovascular diseases. The aim of present study was to explore effects of prolonged administration of QCT on changes induced by repeated application of doxorubicin (DOX) in rat hearts.

Chronic cardiotoxicity of doxorubicin involves activation of myocardial and circulating matrix metalloproteinases in rats.

Aim: To investigate the role of matrix metalloproteinases (MMPs) in the responses of rats to a prolonged doxorubicin (DOX) treatment.

Methods: Male Wistar rats were used. DOX was administered by intraperitoneal injections of seven doses (cumulative dose was 15 mg/kg).

Activation of Akt kinase accompanies increased cardiac resistance to ischemia/reperfusion in rats after short-term feeding with lard-based high-fat diet and increased sucrose intake.

High-fat or high-carbohydrate food consumption contributes to changes in myocardial tolerance to ischemia. However, with respect to experimental models, most studies used diets with very high doses of cholesterol, saturated fatty acids, or fructose. In our study, we fed rats a high-fat diet based on lard in combination with administration of a sweet beverage (30% sucrose solution) (high-fat sucrose diet [HFS]).

The effect of chronic doxorubicin treatment on mitogen-activated protein kinases and heat stress proteins in rat hearts.

The study has been designed to characterize protein systems involved in the responses of rat hearts to chronic doxorubicin (DOX) treatment. We investigated the influence of DOX on cardiac function, mitogen-activated protein kinases (MAPKs) and heat stress proteins (HSPs). Doxorubicin was administered to rats by intraperitoneal injections over a period of 6 weeks.

The effect of chronic nitric oxide synthases inhibition on regulatory proteins in rat hearts.

The aim of the present study was to characterize the effects of chronic nitric oxide synthase (NOS) inhibition on the alterations of regulatory myocardial proteins of intracellular signaling pathways (mitogen-activated protein kinase (MAPK) and Akt kinase cascades) and matrix metalloproteinases (MMP). Chronic NO deficiency (NOD) was induced by NG-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day, 4 weeks). Protein levels and activation of protein kinases were determined using specific antibodies, activities of MMP were analyzed by zymography in gels containing gelatin as a substrate.