Risk Evaluation in Action for Cardiovascular Health

Gilski, Donna; Borkenhagen, Brenda

doi:10.4037/ccn2005.25.1.26

Cited by 16 publications

(2 citation statements)

References 14 publications

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“…Cardiovascular diseases (CVD) will be the most important cause of mortality in India by the year 2015 1. The cardiovascular system is susceptible to many chronic diseases such as hypertension and myocardial infarction (MI).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Protective effects of caffeic acid on lactate dehydrogenase isoenzymes, electrocardiogram, adenosine triphosphatases, and hematology on isoproterenol‐induced myocardial infarcted rats

Kumaran

Prince

2011

J Biochem & Molecular Tox

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The present study aims to evaluate the protective effects of caffeic acid on isoproterenol-treated myocardial infarction. Male albino Wistar rats were pretreated with caffeic acid (15 mg/kg) daily for 10 days. After the pretreatment, rats were injected with isoproterenol (100 mg/kg) at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-treated rats showed increased intensity of lactate dehydrogenase-1 and 2 isoenzyme bands and elevated ST segments. The activity of the heart sodium potassium adenosine triphosphatase was decreased, and the activities of the heart magnesium adenosine triphosphatase and calcium adenosine triphosphatase were increased in isoproterenol-treated rats. Isoproterenol-treated rats also showed a significant increase in the concentration of heart calcium. Furthermore, it significantly increased the counts of red blood cells, hemoglobin, white blood cells, and neutrophils and decreased significantly the concentration of erythrocyte sedimentation rate and the counts of lymphocytes and eosinophils. Pretreatment with caffeic acid showed protective effects on all the biochemical parameters, hematology and minimized alterations in lactate dehydrogenase isoenzymes and electrocardiogram. In vitro study confirmed the free radical scavenging potential of caffeic acid. The observed effects might be due to the free radical scavenging and membrane-stabilizing property of caffeic acid.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Protective effects of caffeic acid on lactate dehydrogenase isoenzymes, electrocardiogram, adenosine triphosphatases, and hematology on isoproterenol‐induced myocardial infarcted rats

Kumaran

Prince

2011

J Biochem & Molecular Tox

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“…It is an acute necrotic state occurring because of imbalance between cardiac blood supply and demand [1]. It is a major health problem in both developing and developed countries, making large interest to the mortality data [2]. Different studies have proposed that over-activity of renin-angiotensin-aldosterone system (RAAS) plays a crucial role in the pathogenesis of MI [3,4].…”

Section: Introductionmentioning

confidence: 99%

Renin Inhibition by Aliskiren Protects Rats Against Isoproterenol Induced Myocardial Infarction

et al. 2017

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

Kumaran

Prince

2010

Cell Stress and Chaperones

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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. After the pretreatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed considerable increased levels of serum troponins and heart mitochondrial lipid peroxidation products and considerable decreased glutathione peroxidase and reduced glutathione. Also, considerably decreased activities of isocitrate, succinate, malate, α-ketoglutarate, and NADH dehydrogenases and cytochrome-C-oxidase were observed in the mitochondria of myocardial-infarcted rats. The mitochondrial calcium, cholesterol, free fatty acids, and triglycerides were considerably increased and adenosine triphosphate and phospholipids were considerably decreased in isoproterenol-induced rats. Caffeic acid pretreatment showed considerable protective effects on all the biochemical parameters studied. Myocardial infarct size was much reduced in caffeic acid pretreated isoproterenol-induced rats. Transmission electron microscopic findings also confirmed the protective effects of caffeic acid. The possible mechanisms of caffeic acid on cardiac mitochondria protection might be due to decreasing free radicals, increasing multienzyme activities, reduced glutathione, and adenosine triphosphate levels and maintaining lipids and calcium. In vitro studies also confirmed the free-radicalscavenging activity of caffeic acid. Thus, caffeic acid protected rat's heart mitochondria against isoproterenolinduced damage. This study may have a significant impact on myocardial-infarcted patients.

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Risk Evaluation in Action for Cardiovascular Health

Cited by 16 publications

References 14 publications

RETRACTED: Protective effects of caffeic acid on lactate dehydrogenase isoenzymes, electrocardiogram, adenosine triphosphatases, and hematology on isoproterenol‐induced myocardial infarcted rats

RETRACTED: Protective effects of caffeic acid on lactate dehydrogenase isoenzymes, electrocardiogram, adenosine triphosphatases, and hematology on isoproterenol‐induced myocardial infarcted rats

Renin Inhibition by Aliskiren Protects Rats Against Isoproterenol Induced Myocardial Infarction

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

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