Cardioprotective effects of p-coumaric acid on tachycardia, inflammation, ion pump dysfunction, and electrolyte imbalance in isoproterenol-induced experimental myocardial infarction.

Cardiovascular diseases cause a large number of deaths throughout the world. No research was conducted earlier on p-coumaric acid's effect on tachycardia, inflammation, ion pump dysfunction, and electrolyte imbalance. Hence, we appraised the above-said parameters in isoproterenol-induced myocardial infarcted rats.

β-caryophyllene blocks reactive oxygen species-mediated hyperlipidemia in isoproterenol-induced myocardial infarcted rats.

Myocardial infarction (MI) is a leading cause of death. Lipid-lowering interventions have been shown to decrease coronary events and mortality of MI and heart failure. In this investigation, we assessed the anti-hyperlipidemic effects of β-caryophyllene in isoproterenol-induced myocardial infarcted rats.

Protective effects of β-caryophyllene on mitochondrial damage and cardiac hypertrophy pathways in isoproterenol-induced myocardial infarcted rats.

The cardiac mitochondrial damage and cardiac hypertrophy pathways are intimately associated with the pathology of myocardial infarction (MI). The protective effects of β-caryophyllene on mitochondrial damage and cardiac hypertrophy pathways in isoproterenol-induced myocardial infarcted rats were investigated. Isoproterenol (100 mg/kg body weight) was administered to induce MI.

β-caryophyllene modulates B-cell lymphoma gene-2 family genes and inhibits the intrinsic pathway of apoptosis in isoproterenol-induced myocardial infarcted rats; A molecular mechanism.

Myocardial infarction (MI) is one of the top causes of morbidity and mortality in the world. Prevention/treatment of MI is of utmost importance. This study planned to appraise the molecular mechanisms of β-caryophyllene on the intrinsic pathway of cardiomyocyte apoptosis in isoproterenol-induced myocardial infarcted rats.

Preventive effects of (-) epicatechin on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in isoproterenol-induced myocardial infarcted rats.

Myocardial infarction (MI) is a life-threatening condition. No studies were conducted earlier on the effects of (-) epicatechin (EC) on tachycardia, cardiac hypertrophy, and inflammation in MI. Hence, the preventive effects of EC on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in experimental MI were appraised.

β-Caryophyllene inhibits Fas- receptor and caspase-mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction.

We planned to appraise the effects of β-caryophyllene on Fas- receptor and caspase-mediated apoptosis signaling pathway and endothelial dysfunction in rats infarcted with isoproterenol. Rats were induced myocardial infarction by using isoproterenol (100 mg/kg body weight [b.w]).

A molecular mechanism on the antiapoptotic effects of zingerone in isoproterenol induced myocardial infarcted rats.

Myocardial infarction continues to be a major public health problem, not only in western countries but also increasingly in developing countries and makes significant contribution to the mortality statistics. Reduction in mortality and prevention of myocardial infarction are of utmost importance. Recently, there has been an increased interest globally to identify natural compounds that are pharmacologically potent and have low or no adverse effects for use in preventive medicine.

Diosmin prevents left ventricular hypertrophy, adenosine triphosphatases dysfunction and electrolyte imbalance in experimentally induced myocardial infarcted rats.

Currently, there has been an increased interest globally to identify natural compounds that are pharmacologically potent and have low or no adverse effects for use in preventive medicine. Myocardial infarction is a vital pathological feature resulting in high levels of mortality and morbidity. Left ventricular hypertrophy (LVH), adenosine triphosphatases (ATPases) dysfunction and electrolyte imbalance play a vital role in the pathogenesis of myocardial infarction.

Vanillic acid prevents altered ion pumps, ions, inhibits Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in myocardial infarcted rats.

The present study aims to evaluate the preventive effects of vanillic acid on altered ion pumps, ions and Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with vanillic acid (5 mg/kg and 10 mg/kg body weight) daily for 10 days. After the pretreatment, isoproterenol (100 mg/kg body weight) was injected into rats at an interval of 24h for 2 days to induce myocardial infarction.

A biochemical and 2, 3, 5-triphenyl tetrazolium chloride staining study on the preventive effects of zingerone (vanillyl acetone) in experimentally induced myocardial infarcted rats.

Myocardial infarction continues to be a major public health problem, not only in western countries but also increasingly in developing countries and makes significant contribution to the mortality statistics. Reduction in mortality rate and prevention of myocardial infarction are of utmost importance. Tachycardia, left ventricular hypertrophy (LVH), altered adenosine triphosphatases (ATPases), and shifts in electrolyte balance play a vital role in the pathogenesis of myocardial infarction.

(-) Epicatechin prevents alterations in lysosomal glycohydrolases, cathepsins and reduces myocardial infarct size in isoproterenol-induced myocardial infarcted rats.

The preventive effects of (-) epicatechin on oxidative stress, cardiac mitochondrial damage, altered membrane bound adenosine triphosphatases and minerals were reported previously in isoproterenol-induced myocardial infarction model. Leakage of lysosomal glycohydrolases and cathepsins play an important role in the pathology of myocardial infarction. This study was aimed to evaluate the preventive effects of (-) epicatechin on alterations in lysosomal glycohydrolases, cathepsins and myocardial infarct size in isoproterenol-induced myocardial infarcted rats.

Protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats.

In the pathology of myocardial infarction, lysosomal lipid peroxidation and resulting enzyme release play an important role. We evaluated the protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats. Male Wistar rats were treated with sinapic acid (12 mg/kg body weight) orally daily for 10 days and isoproterenol (100 mg/kg body weight) was injected twice at an interval of 24 h (9th and 10th day).

Protective effects of thymol on altered plasma lipid peroxidation and nonenzymic antioxidants in isoproterenol-induced myocardial infarcted rats.

This study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)-induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg/kg body weight) daily for 7 days.

Preventive effects of N-acetyl cysteine on lipids, lipoproteins and myocardial infarct size in isoproterenol induced myocardial infarcted rats: an in vivo and in vitro study.

The present study evaluated the preventive effects of N-acetyl cysteine in isoproterenol induced myocardial infarcted rats. Rats were pretreated with N-acetyl cysteine (10 mg/kg body weight) daily for a period of 14 days. After pretreatment, rats were injected with isoproterenol (100 mg/kg body weight) at an interval of 24 h for two days to induce myocardial infarction.

A biochemical, electrocardiographic, electrophoretic, histopathological and in vitro study on the protective effects of (-)epicatechin in isoproterenol-induced myocardial infarcted rats.

(-) Epicatechin rich foods and (-) epicatechin improve cardiovascular function. Consumption of diets rich in flavonoids is associated with reduced risk of cardiovascular diseases. Oxidative stress resulting from increased production of free radicals associated with decreased levels of antioxidants in the myocardium plays a major role in the pathogenesis of myocardial infarction.

Protective effects of vanillic acid on electrocardiogram, lipid peroxidation, antioxidants, proinflammatory markers and histopathology in isoproterenol induced cardiotoxic rats.

Myocardial infarction affects a large proportion in the world. This study aims to evaluate the protective effects of vanillic acid in isoproterenol induced cardiotoxic rats. Male Wistar rats were pretreated with vanillic acid (5mg and 10mg/kg) daily for 10 days.

Protective effects of N-acetyl cysteine on lipid peroxide metabolism on isoproterenol-induced myocardial infarcted rats.

The present study was designed to evaluate the preventive effects of N-acetyl cysteine on lipid peroxide metabolism in isoproterenol (ISO) induced myocardial infarcted rats. Male albino Wistar rats were pretreated with N-acetyl cysteine (5 and 10 mg/kg) daily for a period of 14 days. After the pretreatment period, ISO (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h.

Antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic Wistar rats.

The present study aims to evaluate the antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic male Wistar rats. To induce diabetes mellitus, rats were injected with streptozotocin intraperitoneally at a single dose of 40mg/kg. Streptozotocin induced diabetic rats showed significant (P<0.

Preventive effects of rutin on lysosomal enzymes in isoproterenol induced cardio toxic rats: biochemical, histological and in vitro evidences.

This study was aimed to evaluate the preventive effect of rutin on lysosomal enzymes in isoproterenol induced cardio toxic rats. Male albino Wistar rats were pretreated with rutin (80 mg/kg) daily for a period of 42 days. After the pretreatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for two days.

Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage.

Cardiac mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. The protective effects of caffeic acid on mitochondrial dysfunction in isoproterenol-induced myocardial infarction were studied in Wistar rats. Rats were pretreated with caffeic acid (15 mg/kg) for 10 days.

Pretreatment with quercetin ameliorates lipids, lipoproteins and marker enzymes of lipid metabolism in isoproterenol treated cardiotoxic male Wistar rats.

Lipids and lipoproteins play an important role in the pathology of myocardial infarction. This manuscript reports the preventive effect of quercetin on lipids, lipoproteins and electrocardiogram in isoproterenol treated cardiotoxic male Wistar rats. Quercetin (10mg/kg) was administered orally as pretreatment to Wistar rats daily for seven days.

Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats.

This study was aimed to evaluate the preventive effect of gallic acid on lysosomal enzymes in isoproterenol treated myocardial infarcted rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h.

Preventive effect of S-allylcysteine on membrane-bound enzymes and glycoproteins in normal and isoproterenol-induced cardiac toxicity in male Wistar rats.

This study was aimed to evaluate the preventive role of S-allylcysteine (SAC) on creatine kinase-MB, iron, iron binding capacity, uric acid, total protein, membrane-bound enzymes such as sodium potassium-dependent adenosine triphosphatase, calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase, and glycoproteins such as hexose, hexosamine, fucose and sialic acid in isoproterenol-induced myocardial infarction in rats. Male albino Wistar rats were pre-treated with SAC (50, 100 and 150 mg/kg) daily for a period of 45 days. After the treatment period, isoproterenol (150 mg/kg) was subcutaneously injected in rats at an interval of 24 hr for 2 days.

Cardioprotective effect of 'Marutham' a polyherbal formulation on isoproterenol induced myocardial infarction in Wistar rats.

Myocardial infarction is the number one killer disease in many parts of the world. The cardioprotective effect of Marutham, a polyherbal formulation on serum and heart tissue lipids, serum lipoproteins and heart membrane bound enzymes in isoproterenol induced myocardial infarction was studied in Wistar rats. Pretreatment with Marutham at different doses of 30, 60 and 90 mg kg(-1) to isoproterenol treated rats significantly prevented the altered lipid profile and membrane bound enzymes to near normal status.