Isoproterenol-induced Myocardial Infarction In Rats Research Articles

Ellagic acid inhibits cardiac arrhythmias, hypertrophy and hyperlipidaemia during myocardial infarction in rats

ObjectiveThe objective was to evaluate the protective effect of ellagic acid against experimentally induced cardiac arrhythmias, hypertrophy and its association with altered lipid metabolism during myocardial infarction in rats. MethodsRats were treated with ellagic acid (7.5 and 15mg/kg) orally for a period of 10days. After 10days of pretreatment, isoproterenol (100mg/kg) was injected subcutaneously at an interval of 24h for 2days to induce myocardial infarction. On the 12th day, the cardiac rhythm was observed. The rats were sacrificed and the heart was isolated from each rat. Ventricular hypertrophy and myocardial necrotic scores were analysed in the myocardium. Lipid peroxidation products in the plasma were analysed. Changes in the lipid profile were measured using the plasma and heart tissue homogenates of normal and experimental rats. ResultsIsoproterenol-induced rats showed arrhythmias, hypertrophy and increased levels of myoglobin, creatine kinase-MB, lipid peroxidation products compared to the normal control rats. Ventricular hypertrophy and increased myocardial necrotic scores were observed in isoproterenol-induced rats. Oral pretreatment with ellagic acid restored pathological arrhythmias, ventricular hypertrophy, lipid peroxidation, altered lipid profile and myocardial necrosis in the isoproterenol-induced myocardial infarcted rats. ConclusionsOral pretreatment with ellagic acid was safe and effective in cardio protection against ISO-induced arrhythmias, hypertrophy and myocardial necrosis. Anti lipid peroxidation property and anti hyperlipidaemic activity through 3-hydroxy-3 methyl glutaryl CoA reductase inhibition by ellagic acid may be the reasons for the beneficial action of ellagic acid against experimentally induced myocardial infarction.

Morin protects heart from beta-adrenergic-stimulated myocardial infarction: an electrocardiographic, biochemical, and histological study in rats

In recent years, polyphenols have attracted considerable attention as agents that protect cells or molecules from oxidative myocardial injury. The aim of the study was to prove the cardioprotective benefits of the flavonoid morin in isoproterenol-induced myocardial infarcted rats. Male Wistar rats are treated orally with morin (10 and 20 mg/kg) daily for a period of 21 days. After 21 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days to induce myocardial infarction. Electrocardiographical abnormalities and biomarkers were measured in normal and experimental rats. Isoproterenol-induced myocardial infarcted rats showed significant (p<0.05) increase in the levels of cardiac markers. Pretreatment with morin regulated the abnormalities in electrocardiograph and biomarkers. The lipid peroxidation products were increased and indicated the increased lipid peroxidation in isoproterenol-induced myocardial infarcted rats. The rats pretreated with morin significantly reduced lipid peroxidation. The altered lipid metabolism was observed in isoproterenol-induced myocardial infarcted rats and in pretreatment with morin-regulated lipid metabolism. Histopathological study evidenced that the pretreatment with morin inhibited myocardial damage. The results of this study proved the protective effect of morin as pretreatment and are rational to understand the beneficial effects of morin on cardioprotection against myocardial injury. Based on the results, the cardioprotective ability of morin on human beings can be studied in the future.

Coptisine exert cardioprotective effect through anti-oxidative and inhibition of RhoA/Rho kinase pathway on isoproterenol-induced myocardial infarction in rats

ObjectiveBecause myocardial infarction is a major cause of morbidity and mortality worldwide, protecting the heart from the ischemia is the focus of intense research. Coptisine is an isoquinoline alkaloid extracted form Coptidis Rhizoma. This study aims to elucidate if coptisine is responsible for cardioprotection using myocardial infarction (MI) rat models and investigate its potential mechanism of action. MethodsMyocardial infarction was produced in rats with 85mgkg−1 isoproterenol administered subcutaneously twice at an interval of 24h. The rats were randomized into 7 groups: (I) Normal; (II) ISO; (III) ISO+fasudil; (IV) ISO+isosorbide dinitrate (ISDN) and (V–VII) ISO+coptisine (25, 50 and 100mgkg−1). Cardiac function and markers of cardiac ischemic were assessed after MI. ResultsRats pretreated with coptisine (25, 50 and 100mgkg−1) for 21 days and received subcutaneously injected with ISO (85mgkg−1) on the 20th and 21st day at an interval of 24h. The results suggested that coptisine has strong antioxidant activity, and it can maintain cell membrane integrity, ameliorate mitochondrial respiratory dysfunction, reduce myocardial cells apoptosis, inhibit RhoA/ROCK expression induced by high-dose isoproterenol administration. ConclusionsCoptisine provided cardioprotection in a model of myocardial infarction, and therefore should be considered as a novel adjunctive therapy for attenuating myocardial damage.

Cardioprotective effect of HPLC standardized ethanolic extract of Terminalia pallida fruits against isoproterenol-induced myocardial infarction in albino rats

Ethnopharmacological relevanceTerminalia pallida is an evergreen endemic tree, mentioned in Ayurveda as the fruits of Terminalia pallida are excellent in cardioprotective property. Tribal people use Terminalia pallida fruit for the treatment of diabetes and this plant widely used in many other disorders. Aim of studyThe present investigation was to evaluate the antioxidant, biochemical profile and histological studies of qualitatively standardized ethanolic extract of Terminalia pallida fruits (TpFE) against isoproterenol-induced myocardial infarction in rats. Materials and methodsTpFE was standardized by high performance liquid chromatography (HPLC) and mass spectroscopy (MS). Rats were pretreated orally with different doses of TpFE (100, 300, and 500mgkg−1 body weight) and cardioprotective positive control gallic acid (GA) for 30 days prior to isoproterenol (ISO) induced myocardial infarction. The rats were sacrificed, hearts were collected and homogenized for biochemical analysis. The effects on total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C), high density lipoprotein cholesterol (HDL-C), lipid peroxidation (LPO) marker, malondialdehyde (MDA), creatine kinase (CK), lactate dehydrogenase (LDH), alanine transaminase (ALT), aspartate transaminase (AST), catalase (CAT), glutathione peroxidase (GPx), sodium potassium (Na+/K+), calcium (Ca2+) and magnesium (Mg2+) adenosine triphosphatases (ATPases) were estimated in heart tissue homogenate. ResultsRats administered with ISO showed a significant increase in TC, TG, LDL-C, VLDL-C, and MDA and a significant decrease in HDL-C, cardiac marker enzymes – CK, LDH, ALT and AST. ISO significantly reduced antioxidants – CAT, GPx, and membrane bound enzymes – Na+/K+, Ca2+ and Mg2+ ATPases. Pretreatment with TpFE (100, 300, and 500mgkg−1 bw) and GA (15mgkg−1 bw) for a period of 30 days significantly inhibited the effects of ISO. Moreover, biochemical findings were supported by histopathological observations. ConclusionThe present study provide evidence for the first time, that TpFE pretreatment ameliorated myocardial injury in ISO-induced myocardial infarcted rats and exhibited cardioprotective activity.

Cardio Protective Effect of Vitamin A against Isoproterenol-Induced Myocardial Infarction

Vitamin A is beneficial in counteracting free radical damage, therefore the present study is designed to investigate the effect of vitamin A against isoproterenol-induced myocardial infarction in rats. Male Wistar rats were divided into three groups, namely a normal control group, an isoproterenol group (150 mg/kg, s.c.), and a vitamin A treatment (4,500 IU/kg/d, orally) group. Vitamin A-treated rats demonstrated significant reduction in ST-segment (p<0.001) and infarct sizes (p<0.05) when compared with the isoproterenol group of rats, suggesting that vitamin A markedly attenuated myocardial injury. Vitamin A treatment resulted in a significant decrease in the serum level of troponin I (p<0.001), creatinine kinase-MB (p<0.01), creatine kinase (p<0.05), lactate dehydrogenase (p<0.05), aspartate aminotransferase (p<0.01) and alanine aminotransferase (p<0.01). Vitamin A treatment resulted in a significant decrease in malondialdehyde (p<0.001), and significant increases were observed in reduced glutathione (p<0.01), superoxide dismutase (p<0.05) and catalase (p<0.001). Vitamin A treatment resulted in a significantly increased level of Na(+)-K(+) ATPase (p<0.05) and Mg(2+)-ATPase (p<0.01) and a significant reduction of Ca(2+) ATPase (p<0.01). Vitamin A treatment also demonstrated a significantly decreased level of C-reactive protein (p<0.05) and myeloperoxidase activity (p<0.01). In conclusion, vitamin A attenuated the myocardial infarction and prevention was shown via membrane stabilization, reduction in oxidative stress, and prevention of neutrophil infiltration.

Cardioprotective effect of Spathodea campanulata bark on isoproterenol-induced myocardial infarction in rats

ObjectiveTo evaluate the cardioprotective potential of 70% ethanolic extract of bark of Spathodea campanulata P. Beauv (EEBSC). MethodsWister strain rats were pretreated with EEBSC in two different doses (250 and 500 mg/kg) orally for 14 d and then intoxicated with isoproterenol (200 mg/kg, s.c. for 2 consecutive days at an interval of 24 h on 14th and 15th day of treatment protocol) to induce myocardial injury. ResultsCardioprotection was assessed by estimating serum aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, triglycerides, total cholesterol, low density lipoproteins and high density lipoproteins. The levels of thiobarbituric acid reactive substances and reduced glutathione were analyzed in heart homogenate. In isoproterenol-treated group, shrinkage of cardiac markers in serum and elevated lipid peroxidation accompanied by decreased content of reduced glutathione in heart. The prior administration of EEBSC significantly (P < 0.05) prevented the isoproterenol-induced alterations and restored the cardiac markers. The observed results were further confirmed by histopathological findings. ConclusionsThese findings indicate that EEBSC exerts cardioprotective effect against isoproterenol induced myocardial infarction due to its free radical scavenging effects, which maintains the tissue defence system against myocardial damage.

Coconut haustorium maintains cardiac integrity and alleviates oxidative stress in rats subjected to isoproterenol-induced myocardial infarction

The present study evaluates the effect of aqueous extract of coconut haustorium on isoproterenol-induced myocardial infarction in Sprague Dawley rats. Rats were pretreated with aqueous extract of coconut haustorium (40 mg/100 g) orally for 45 days. After pretreatment, myocardial infarction was induced by injecting isoproterenol subcutaneously (20 mg/100 g body weight) twice at an interval of 24 h. Activity of marker enzymes like lactate dehydrogenase, creatinine kinase-MB, aspartate transaminase and alanine transaminase were increased in the serum and decreased in the heart of isoproterenol treated rats indicating cardiac damage. These changes were significantly reduced in haustorium pretreated rats. Moreover, an increase in the activities of antioxidant enzymes and decrease in the levels of peroxidation products were observed in the myocardium of coconut haustorium pretreated rats. Histopathology of the heart of these rats showed almost normal tissue morphology. From these results, it is clear that aqueous extract of coconut haustorium possess significant cardioprotective and antioxidant properties during isoproterenol-induced myocardial infarction in rats.

Litsea Deccanensis Ameliorates Myocardial Infarction in Wistar Rats: Evidence from Biochemical Histological Studies

The present study was designed to evaluate the cardioprotective effects of methanolic extract of Litsea deccanensis (MELD) against isoproterenol-induced myocardial infarction in rats by studying cardiac markers, lipid peroxidation, lipid profile, and histological changes. Male Wistar rats were treated orally with MELD (100 and 200 mg/kg) daily for a period of 21 days. After 21 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed significant (P < 0.05) increase in the levels of serum creatine kinase, lactate dehydrogenase, thiobarbituric acid reactive substances, and lipid hydro peroxides. The serum lipid levels were altered in the isoproterenol-induced myocardial infarcted rats. The histopathological findings of the myocardial tissue evidenced myocardial damage in isoproterenol-induced rats. The oral pretreatment with MELD restored the pathological alterations in the isoproterenol-induced myocardial infarcted rats. The MELD pretreatment significantly reduced the levels of biochemical markers, lipid peroxidation and regulated the lipid profile of the antioxidant system in the isoproterenol-induced rats. An inhibited myocardial necrosis was evidenced by the histopathological findings in MELD pretreated isoproterenol-induced rats. Our study shows that oral pretreatment with MELD prevents isoproterenol-induced oxidative stress in myocardial infarction. The presence of phenolic acid and flavonoid contents were confirmed by preliminary phytochemical tests. The reducing power and free radical scavenging activities of the MELD may be the possible reason for it pharmacological actions.

Cardioprotective Effects of Lagenaria siceraria Fruit Juice on Isoproterenol-induced Myocardial Infarction in Wistar Rats: A Biochemical and Histoarchitecture Study

The present study was designed to evaluate the cardioprotective effects of Lagenaria siceraria fruit juice in isoproterenol-induced myocardial infarction. Rats injected with isoproterenol (200 mg/kg, s.c.) showed a significant increase in the levels of serum uric acid, tissue Na++ and Ca++ ions and membrane-bound Ca+2-ATPase activity. A significant decrease in the levels of serum protein, tissue K+ ion, vitamin E level, and the activities of Na+/K+-ATPase and mg+2-ATPase was observed. Isoproterenol injected rats also showed a significant increase in the intensity of lactate dehydrogenase isoenzyme and histopathologic alterations in the heart. Treatment with L. siceraria fruit juice (400 mg/kg/day, p.o.) for 30 days and administration of isoproterenol on 29th and 30th days showed a protective effect on altered biochemical and histopathologic changes. These findings indicate the cardioprotective effect of L. siceraria fruit juice in isoproterenol-induced myocardial infarction in rats.

Ellagic acid protects mitochondria from β-adrenergic agonist induced myocardial damage in rats; evidence from in vivo, in vitro and ultra structural study

This study aimed to evaluate the protective role of ellagic acid against mitochondrial damage in beta adrenergic agonist (isoproterenol)-induced myocardial infarction in Wistar rats in order to provide a scientific basis for the use of ellagic acid in preventing myocardial infarction. Mitochondria were isolated from the heart tissue of rats from all the groups. Lipid profile, lipid peroxidation, antioxidant enzyme activities and mitochondrial enzyme activities were measured. The structure of mitochondria was analysed by transmission electron microscopy. Isoproterenol-induced rats showed a significant increase in mitochondrial lipid peroxidation products and alterations in mitochondrial lipid profile. Significant decreases in mitochondrial antioxidants and tricarboxylic acid cycle enzymes were also found in the heart mitochondria of isoproterenol-induced myocardial infarcted rats. The protective effect of ellagic acid on the heart mitochondrial structure was evidenced by transmission electron microscopic study. Free radical scavenging and metal chelating activities of ellagic acid which are confirmed by in vitro studies may be the mechanism, responsible for the protective action against mitochondrial damage in myocardial infarction. The results support the importance of ellagic acid in regular diet to prevent 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. This study aims to evaluate the preventive effects of (-) epicatechin on oxidative stress in isoproterenol-induced myocardial infarcted rats. Male Wistar rats were pretreated with (-) epicatechin (20mg/kg body weight) daily for 21 days. After pretreatment, isoproterenol (100mg/kg body weight) was injected into the rats at an interval of 24h for two days to induce myocardial infarction. Isoproterenol induced rat's electrocardiogram showed elevated ST segments and significant increase in the activity of serum creatine kinase-MB, level of serum troponin-T and increased intensities of serum lactate dehydrogenase 1 and 2-isoenzymes. The rats also showed significant increased levels of heart lipid peroxidation products and significant decreased activities of heart superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and levels of reduced glutathione. Pretreatment with (-) epicatechin revealed significant protective effects on all the biochemical parameters and electrocardiogram investigated. Histopathology of myocardium confirmed the present findings. The in vitro study on the effects of (-) epicatechin on scavenging free radical 1,1-diphenyl-2-picrylhydrazyl revealed the free radical scavenging potential of (-) epicatechin. Thus, (-) epicatechin exerts protective effects against isoproterenol-induced oxidative stress thereby reducing cardiac tissue damage by its free radical scavenging and antioxidant effects.

Cardioprotective effect of safranal on isoproterenol-induced myocardial infarction in rat

Cardioprotective effect of safranal on isoproterenol-induced myocardial infarction in rat

Ganoderma lucidum ameliorate mitochondrial damage in isoproterenol-induced myocardial infarction in rats by enhancing the activities of TCA cycle enzymes and respiratory chain complexes

BackgroundDecreased mitochondrial function has been suggested to be one of the important pathological events in isoproterenol (ISO)-induced cardiotoxicity. In this communication, we have evaluated the protective effect of Ganoderma lucidum against ISO induced cardiac toxicity and mitochondrial dysfunction. MethodsCardiac toxicity was assessed by determining the activities of creatine kinase (CK) and lactate dehydrogenases (LDH) after subcutaneous injection of ISO (85mg/kg) at an interval of 24h for 2days. The animals were sacrificed 24h after last ISO administration. G. lucidum (100 and 250mg/kg, p.o.) was given to the rats once daily for 15days prior to the ISO challenge. Similarly, α-Tocopherol (100mg/kg, p.o) was kept as the standard. To assess the extent of cardiac mitochondrial damage, the activities of Krebs cycle dehydrogenases and mitochondrial complexes I, II, III, and IV as well as the level of ROS and mitochondrial membrane potential (ΔΨmt) were evaluated. ResultsAdministration of G. lucidum and α-tocopherol significantly protected the elevated activities of CK and LDH. Further, the activities of mitochondrial enzymes and the level of ΔΨmt were significantly enhanced and the level of ROS was significantly declined in the G. lucidum and α-tocopherol treatments. ConclusionThe present study concluded that the cardiac mitochondrial enzymes are markedly declined by the ISO challenge and the administration G. lucidum and α-Tocopherol significantly protected mitochondria by preventing the decline of antioxidant status and ΔΨmt or by directly scavenging the free radicals.

Mechanistic Clues in the Protective Effect of Ellagic Acid Against Apoptosis and Decreased Mitochondrial Respiratory Enzyme Activities in Myocardial Infarcted Rats

Our previous study described the cardioprotective effects of ellagic acid in an isoproterenol-induced myocardial infarction model. In this study, we are reporting the mechanism of protective action of ellagic acid with respect to apoptosis and mitochondrial respiratory enzymes. Ellagic acid (7.5 and 15mg/kg) was administered orally as a pretreatment for 10days. Then, isoproterenol (100mg/kg) was injected subcutaneously to rats at an interval of 24h for 2days. Myocardial infarction was quantified by planimetry. Apoptosis was measured by apoptotic gene expressions. The levels of mitochondrial respiratory enzymes were also measured. Isoproterenol-induced myocardial infarcted rats showed increased infarct size, a decrease in myocardial expression of the Bcl-2 gene and an increase in myocardial expression of the BAX gene. Fas ligand and caspases were markedly elevated along with compromised respiratory marker enzymes in isoproterenol-induced rats. Ellagic acid pretreatment reduced the infarct size, regulated apoptotic gene expressions and enhanced the activities of mitochondrial respiratory marker enzymes and cell viability, thereby protecting the myocardium against isoproterenol-induced myocardial infarction. The decreased infarct size associated with inhibited apoptosis and increased respiratory marker enzymes provide insight on the role of ellagic acid in antiapoptotic mechanism, and it may be the reason for its cardioprotective activity.

Pharmacodynamics of ellagic acid on cardiac troponin-T, lyosomal enzymes and membrane bound ATPases: Mechanistic clues from biochemical, cytokine and in vitro studies

The anti lipid peroxidative and antioxidant effects of ellagic acid against isoproterenol-induced myocardial infarcted rats were reported previously. This study was designed to evaluate the protective effects of ellagic acid on the levels of cardiac troponin-T, lysosomal enzymes, and membrane bound ATPases along with the role of pro inflammatory cytokine. Male albino Wistar rats were pretreated with ellagic acid (7.5 and 15mg/kg body weight) daily for a period of 10days. After the pretreatment period isoproterenol (100mg/kg) was subcutaneously injected to rats twice at an interval of 24h. The protective effects of pretreatment with ellagic acid were measured by biochemical analysis and reverse transcriptase polymerase chain reaction. Evidence of myocardial infarction in isoproterenol induced rats included significant increase in the serum level of cardiac troponin-T and decreased levels of creatine kinase and lactate dehydrogenase in heart tissue homogenate .The pretreatment with ellagic acid restored the levels of cardiac markers in the serum and heart tissue homogenates. The activities of lysosomal enzymes (β-d-glucuronidase, β-N-acetyl glucosaminidase, β-galactosidase, cathepsin-d and acid phosphatase) were increased significantly in the serum and heart tissue of isoproterenol-induced rats. The activity of Na+/K+ATPase declined while the activities of Ca2+ATPase and Mg2+ATPase were increased significantly in the heart of isoproterenol-induced rats. Pretreatment with ellagic acid restored the activities of lysosomal enzymes and membrane bound ATPases. The higher expressions of pro-inflammatory cytokines such as interleukin-1β, interleukin-6 and tumour necrosis factor-α in the isoproterenol-induced rats were controlled by the pretreatment with ellagic acid. Our results imply that oral pretreatment with ellagic acid protects the heart lysosomal membrane against isoproterenol-induced cardiac damage. The observed effects might be due to the free radical scavenging, membrane stabilizing and anti-inflammatory properties of ellagic acid.

Pretreatment with morin, a flavonoid, ameliorates adenosine triphosphatases and glycoproteins in isoproterenol-induced myocardial infarction in rats

The aim of this investigation was to evaluate the preventive role of morin, a flavonoid, on cardiac marker enzymes such as aspartate transaminase, lactate dehydrogenase, creatine kinase and creatine kinase-MB, 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 (ISO)-induced myocardial infarction (MI) in rats. Male albino Wistar rats were pretreated with morin (20, 40 and 80 mg/kg) daily for a period of 30 days. After the treatment period, ISO (85 mg/kg) was subcutaneously injected into the rats at an interval of 24 h for 2 days. ISO-induced rats showed significantly (P < 0.05) increased activities of cardiac marker enzymes in serum and decreased activities in the heart, and increased activities of calcium-dependent adenosine triphosphatase and magnesium-dependent adenosine triphosphatase in the heart, and the activity of sodium potassium-dependent adenosine triphosphatase decreased in the heart. ISO induction also showed a significant increase in the levels of glycoproteins in serum and the heart. Pretreatment with morin (40 mg/kg) daily for a period of 30 days exhibited significant (P < 0.05) effects and altered these biochemical parameters positively compared to the other two doses. Thus, our study shows that morin has a protective role in ISO-induced MI in rats. The observed effects might be due to the free radical-scavenging, antioxidant and membrane-stabilising properties of morin.

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

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.

Cardioprotective effect of fenugreek on isoproterenol-induced myocardial infarction in rats.

Objectives:This study is designed to evaluate the cardioprotective effect of fenugreek on isoproterenol- induced myocardial infarction and is investigated by an in vivo method in rats.Materials and Methods:Male Wistar albino rats were divided into four groups (n=10). Group I received 0.5% CMC treated as normal control group. Group II received isoproterenol (85 mg/kg body weight) intraperitoneal (i.p.) for two consecutive days (14th and 15th days). Group III received fenugreek (250 mg/kg body weight) intragastric intubation for 15 days. Group IV rats received fenugreek as in Group III and additionally isoproterenol was given for two consecutive days (14th and 15th days).Results:The results described the cardioprotective effect that observed in Group IV showed significantly (P< 0.05) decreased levels of TBARS and enhanced the activities of both enzymatic and non-enzymatic antioxidants (SOD, CAT, GPx and GSH) in myocardial infarcted rats when compared to Groups II and III. Histopathological studies were also co-relating with the above biochemical parameters.Conclusion:These findings concluded the cardioprotective effect of fenugreek on lipid peroxidation and antioxidant defense system during isoproterenol-induced myocardial infarction in rats.

The cardioprotective effects of a combination of quercetin and α-tocopherol on isoproterenol-induced myocardial infarcted rats.

The present study aims to evaluate the combined protective effects of quercetin and α-tocopherol on isoproterenol-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with a combination of quercetin (10 mg/kg) and α-tocopherol (10 mg/kg) daily for 14 days. After the pretreatment, rats were injected isoproterenol (100 mg/kg) to induce myocardial infarction. Isoproterenol-treated rats showed increased levels of serum troponins and increased intensities of serum lactate dehydrogenase-1 and -2 isoenzyme bands. Isoproterenol treatment also showed significant decreased levels of antioxidant system and significant increased levels of plasma lipid peroxidation, plasma uric acid, and the heart calcium. Furthermore, isoproterenol-treated rat's electrocardiogram showed elevated ST segments. Combined pretreatment with quercetin and α-tocopherol normalized all the biochemical parameters and minimized the alterations in electrocardiogram. Histopathology of myocardium also confirmed the cardioprotective effects of quercetin and α-tocopherol. In vitro studies confirmed the mechanism of action of quercetin and α-tocopherol. Thus, quercetin and α-tocopherol exhibited cardioprotective effects against isoproterenol-induced cardiotoxicity due to their scavenging free radicals, improving antioxidants and maintaining Ca(2+) levels. Our study also showed that combined pretreatment (quercetin and α-tocopherol) was highly effective than single pretreatment (quercetin or α-tocopherol).

Preventive Effects of Vanillic Acid on Lipids, Bax, Bcl-2 and Myocardial Infarct Size on Isoproterenol-Induced Myocardial Infarcted Rats: A Biochemical and In Vitro Study

We made an attempt to evaluate the preventive effects of vanillic acid on isoproterenol-induced myocardial infarcted rats. Rats were pretreated with vanillic acid (5 and 10 mg/kg) daily for 10 days. After pretreatment, rats were injected with isoproterenol (100 mg/kg) at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol induction increased the activity of serum creatine kinase-MB and increased the levels of serum and heart cholesterol, triglycerides, free fatty acids in rats. It increased the levels of serum low density and very low density lipoprotein cholesterol and decreased the levels of high-density lipoprotein cholesterol. Also, the activity of 3-hydroxy-3methyl glutaryl-coenzyme-A-reductase in the plasma and liver was increased, and lecithin cholesterol acyl transferase activity in the plasma and liver was decreased in isoproterenol-induced rats. Furthermore, isoproterenol-induced rats showed a decrease in myocardial expression of B-cell leukemia/lymphoma-2(bcl-2) gene and an increase in myocardial expression of bcl-2 associated-x (bax)-gene. Vanillic acid pretreated isoproterenol-induced rats positively altered all the above-mentioned biochemical parameters. Vanillic acid pretreatment also reduced myocardial infarct size in myocardial infarcted rats. In vitro study confirmed the potent free radical scavenging effect of vanillic acid. The observed effects are due to free radical scavenging effects of vanillic acid. This study may have a significant impact on myocardial infarcted patients.