Activities Of Cardiac Marker Enzymes Research Articles

Doxorubicin-Induced Cardio Toxicity in Albino Rats Protected by Adansonia Digitata (Baobab) Leaf Extract

Cardiovascular disease is the world's leading cause of death, killing 17 to 19 million people each year. The usage of traditional drugs was influenced by the need for effective medications for the treatment of cardiovascular disease without side effects. The current study investigated the cardio-protective effects of Adansonia digitata leaf extract on doxorubicin-mediated cardiotoxicity in laboratory rats. Thirty-five albino rats were divided into five groups, each consisting of seven rats. Group 1 was given filtered water as a control, while Group 2 was given saline and doxorubicin, Group 3 received doxorubicin and Vitamin E, and Groups IV and V were myocardial oxidative animals treated with Adansonia digitata leaf extract (150 and 300 mg/kg/wt) for two weeks. After the rats were sacrificed, their hearts were collected and homogenized for biochemical assays. The results on the activities of creatinine kinase (CK), lactate dehydrogenase (LDH), aspartate amino transferase (AST), nitric oxide synthase (NOS), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde were determined. Histopathology examination was used in addition to assays to validate myocardial damage. In comparison to the control group, rats provided doxorubicin showed a significant increase in the activities of cardiac marker enzymes (CK, LDH, and AST), as well as a significant increase in malondialdehyde concentration with a concomitant decrease in antioxidant enzymes (SOD, CAT, and NOS), implying cardiotoxicity. In rats with doxorubicin-induced myocardial infection, pretreatment with Adansonia digitata leaf extract reduced myocardial damage, these biochemical results were confirmed by histopathology. Finally, the new study demonstrates that Adansonia digitata has cardioprotective properties.

The cardioprotective effects of the new crystal form of puerarin in isoproterenol-induced myocardial ischemia rats based on metabolomics

Puerarin has shown unique pharmacological effects on myocardial ischemia (MI). Changing the crystal form is an effective approach to improve the cardioprotective effects of puerarin. However, the mechanisms of the new crystal form of puerarin are unclear. In this study, an electrocardiogram, echocardiography, cardiac marker enzymatic activity, oxidative stress indices, and myocardial histology analysis of cardiac tissues were performed to evaluate the cardioprotective effects of the new crystal form of puerarin. Moreover, serum and cardiac tissue metabolomics based on nuclear magnetic resonance (NMR) were used to investigate the potential mechanism of the new crystal form. The results indicated that the new crystal form of puerarin (30 mg/kg) could improve oxidative stress indices, and these improvements were similar to those of the original crystal form of puerarin (120 mg/kg). The new crystal form of puerarin (30 mg/kg) could effectively improve the activities of cardiac marker enzymes, and the improvement effects were better than those of the original crystal form (120 mg/kg). Moreover, metabolomics analysis showed that amino acid metabolism, oxidative stress and energy metabolism were disturbed after MI and could be improved by puerarin. These results demonstrated that the new crystal form of puerarin was effective in treating MI.

Ageratum conyzoides L. Protects rat myocardium during isoproterenol-induced myocardial infarction in rats: A biochemical study

This study aimed to evaluate the preventive effect of Ageratum conyzoides L. on cardiac Troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, blood glucose, total proteins, albumin/globulin (A/G) ratio, serum uric acid, serum iron, and plasma iron binding capacity in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats treated with ISO(85 mg/kg, administered subcutaneously twice at an interval of 24 h for 2 days) showed a significant increase in the degrees of cardiac troponin T (cTnT), the intensity of the bands of LDH1 and LDH2, and the activities of cardiac diagnostic marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST) and alanine transaminase (ALT) in serum with a subsequent decrease in the activities of CK, LDH, AST and ALT in the heart. ISO-induced rats showed a significant increase in blood glucose, serum uric acid, and serum iron and a decrease in the levels of total proteins, A/G ratio, and iron binding capacity. Pre-treatment with A. conyzoides L. (100 and 200 mg/kg) daily for a period of 30 days significantly altered the levels of cTnT, the intensity of the bands of LDH1, and LDH2-isoenzyme and the activities of cardiac marker enzymes, and other biochemical parameters. Thus, A. conyzoides L. possesses a cardioprotective effect in ISO-induced oxidative stress in rats.

Evaluation of the cardioprotective effect of Casuarina suberosa extract in rats

The aim of the current study was to examine and compare the cardioprotective activities of the chloroform and petroleum extracts the leaves of Casuarina suberosa in isoproterenol (ISO)-induced cardiac tissue oxidative stress. Rats were categorized into 6 groups as follows: control group, vehicle or Tween 80-treated group, ISO-treated group, chloroform extract + ISO treated group, petroleum ether extract + ISO treated group and Reference drug (Captopril) + ISO treated group. ISO injection significantly (p < 0.05) increased the activities of cardiac marker enzymes (CK-MB, LDH, ALT, and AST), cardiac troponin-I, levels of lipid peroxides (MDA), nitric oxide (NO), and vascular endothelial growth factor (VEGF), serum angiotensin-converting enzyme (ACE) activity and neutrophil infiltration marker; myeloperoxidase (MPO) in the cardiac tissues. Pretreatment with chloroform or petroleum ether extracts significantly (p < 0.05) prevented the ISO-induced alteration; they upregulated VEGF expression. Histopathological findings corroborated biochemical results. These extracts exerted a cardioprotective effect by alleviating oxidative stress.

Cardioprotective and Hypocholesterolemic Effect of Ethanolic Extract of Mormodicalcharantial in Isoproterenol‐Induced Myocardial Infarction in Adult Wistar Rats

ISO was used to induce MI by intraperitoneal injection at the dose of 100mg/kg to Wistar rats Serum lipid profile and cardiac marker enzymes were obtained and then measured calorimetrically. The results show that isoproterenol‐induced myocardiac infarction were associated with significant (p&lt;0.05) increase in the activities of cardiac marker enzymes in the serum with concomitant decrease in the activities of these enzymes in the myocardial tissue as compared to control group. There were also significant (p&lt;0.05) increase in serum level of total cholesterol , trigyceride, low density lipoprotein and very low density lipoprotein in the group injected with isoproterenol ( group ii) as compared with control group . Pretreatment with leaf extract of Mormodicalcharantial significantly (p&lt;0.05) prevented this alteration of the lipid profile and also of the activities of these cardiac marker enzymes both in the serum and myocardial tissue as compared to isopreterenol‐induced control group. Mormodicalcharantialpossesses cardioprotective effects.Support or Funding InformationThe authors receive no grant for this research but however are grateful to the Department of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Benin, for the use of their research laboratory also acknowledge the technical help of Prof. P.O. Udia , Dept. of Biochemisry, University of Benin, Benin City, Nigeria,This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Alleviation of Cardiac Damage by Dietary Fenugreek (Trigonella foenum-graecum) Seeds is Potentiated by Onion (Allium cepa) in Experimental Diabetic Rats via Blocking Renin-Angiotensin System.

Hyperglycemia is one of the metabolic and homeostatic abnormalities that increase the cardiovascular mortality in diabetic patients by increased oxidative stress. We have recently reported amelioration of oxidative stress in cardiac tissue by dietary fenugreek (Trigonella foenum-graecum) seeds and onion (Allium cepa) in streptozotocin-induced diabetic rats. The mechanistic aspects of the cardio-protective influence of dietary fenugreek seeds (10%) and onion (3% powder) both individually and in combination on hyperglycemia-mediated cardiac damage was further investigated in this study on streptozotocin-induced diabetic rats. Cardio-protective influence of these dietary spices was evidenced by their blocking potential on renin-angiotensin system. This might be the consequence of reduced activation of angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor (AT1) in cardiac tissue. The combination produced an additive effect on ACE and AT1 protein and mRNA expressions. Increased expression of type IV collagen, fibronectin, Bax, 4-hydroxynonenal, iNOS and metabolites of nitric oxide (nitrate/nitrite) along with disturbed PUFA-to-SFA ratio and activities of cardiac marker enzymes in blood confirmed the myocardial damage. Dietary fenugreek seed, onion and fenugreek+onion were found to ameliorate these pathological changes in the cardiovascular system. The beneficial effect being higher with the combination sometime amounting to additive (iNOS expression) or even a synergistic (cardiac Bax and type IV collagen expression and circulatory marker enzymes) in diabetic rats. Thus, the results of present investigation suggested that the combination of fenugreek seeds and onion offers higher beneficial influence in ameliorating cardiac damage accompanying diabetes.

Cardioprotective potential of Dendrobiumofficinale Kimura et Migo against myocardial ischemia in mice.

Dendrobiumofficinale Kimura et Migo has been used for thousands of years to promote body fluid production; however, little is currently known regarding its effects on the heart. The present study aimed to explore the cardioprotective potential of the water extract of Dendrobiumofficinale Kimura et Migo (DOE) on myocardial ischemia in mice. A mouse model of myocardial ischemia was induced following ligation of the left anterior descending coronary artery. Prior to the operation, mice were administered a vehicle or DOE for 2weeks. Following the operation, ST elevation was measured. To estimate the extent of myocardial damage, infarct size analysis and histopathological examination were performed. The activities of cardiac marker enzymes [creatine kinase (CK)‑MB and lactate dehydrogenase (LDH)] and antioxidative indicators [malondialdehyde (MDA) and superoxide dismutase (SOD)] were also analyzed to explore the underlying mechanisms. Treatment with DOE decreased infarct size and the number of apoptotic cardiomyocytes; reduced serum CK‑MB, LDH and MDA activities; and increased SOD levels. According to western blotting, DOE conferred protection against myocardial ischemic injury via the regulation of Meis1 expression. These results indicated that DOE may exert potential cardioprotective effects against myocardial ischemia; these effects may be associated with its antioxidant activity, and its ability to inhibit cardiac cell apoptosis and to regulate Meis1 expression.

Coconut kernel protein in diet protects the heart by beneficially modulating endothelial nitric oxide synthase, tumor necrosis factor-alpha, and nuclear factor-kappaB expressions in experimental myocardial infarction

Previous studies conducted in our laboratory revealed that coconut kernel protein has a significant cardioprotective effect on isoproterenol-induced myocardial infarction in rats. In the present study, we explored the possible protective mechanism of coconut kernel protein during acute myocardial infarction. Coconut kernel protein (50 mg/100 g) was administered to Sprague-Dawley rats orally for 45 days. Isoproterenol (20 mg/100 g) was injected subcutaneously at an interval of 24 hours twice to induce myocardial infarction. Myocardial infarction was confirmed by the abnormal activities of cardiac marker enzymes in serum. Activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase were decreased (p < 0.05) in the heart of isoproterenol-treated rats, whereas pretreatment with coconut kernel protein increased (p < 0.05) these activities. An improved antioxidant status in these rats was further confirmed by the increased level of reduced glutathione and decreased level of lipid peroxidation products. Nitric oxide synthase (NOS) activity in the heart and nitrite level in blood were increased (p < 0.05) in coconut kernel protein-treated rats administered with isoproterenol compared to isoproterenol control rats. Coconut protein pretreatment upregulated the expression of endothelial nitric oxide synthase (eNOS), whereas expressions of nuclear factor-kappaB (NF-κB) and tumor necrosis factor-alpha (TNF-α) were downregulated in isoproterenol-treated rats. These findings suggest that the protective effects of coconut kernel protein may be mediated in part through upregulation of nitric oxide production, antioxidant mechanisms, and its ability to inhibit TNF-α and NF-κB activation.

Luteolin a dietary flavonoid attenuates isoproterenol-induced myocardial oxidative stress in rat myocardium: An in vivo study

Aim of the present study, an attempt has been made in acute and chronic periods after isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Luteolin supplimentated by intragastric intubation at a daily dose of 0.3mg/kg body weight in acute and chronic periods following MI. In acute MI model, luteolin had been administered once per day to rat groups during 30 days. On 29th and 30th day, the rats of the acute MI control groups were administered 85mg/kg body weight, isoproterenol, intraperitoneally intravel of 24h. In chronic MI model, luteolin supplimentated of rat group during 30 days. On the 1st and 2nd days, the rats of the chronic MI control and luteolin treatment groups were administered ISO by the same way. The ISO-induced rats both in acute and chronic models showed decrease in the levels of heart phospholipids and increased levels of cholesterol, triglycerides, free fatty acids and phospholipids in serum and heart, and also significantly increase in the activities of cardiac marker enzymes like Troponin I and T, CK, CK-MB, LDH, AST and ALT. Oral treatment with luteolin at a daily dose of (0.3mg/kg body weight) in both acute and chronic models showed significantly decrease in the levels of heart and serum lipid metabolism products and significant decrease in the levels of marker enzymes. The study results revealed that luteolin ameliorates cardiac damage in ISO-induced myocardial infarction by maintaining lipids levels by its antilipidemic effects in isoproterenol-induced myocardial infarcted rats.

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.

Preventive effect of caffeic acid on lysosomal dysfunction in isoproterenol‐induced myocardial infarcted rats

We evaluated the preventive effect of caffeic acid (CA) on lysosomal enzymes in isoproterenol (ISO)-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with CA (15 mg/kg) daily for a period of 10 days. After the pretreatment period, ISO (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of serum creatine kinase-MB and lactate dehydrogenase was increased significantly (P < 0.05) in ISO-induced myocardial infarcted rats. The levels of plasma thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P < 0.05) increased, and the level of plasma-reduced glutathione was significantly (P < 0.05) decreased in ISO-induced myocardial infarcted rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P < 0.05) in the serum and heart of ISO-induced myocardial infarcted rats. ISO induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in different fractions except cytosol. Pretreatment with CA (15 mg/kg) to ISO-treated rats significantly (P < 0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes in the serum, heart, and subcellular fractions. Oral treatment with CA (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study showed that CA prevented the lysosomal membrane damage against ISO-induced myocardial infarction. The observed effects of CA are due to membrane-stabilizing, antilipo peroxidative, and antioxidant effects.

(—)-Epigallocatechin gallate (EGCG) prevents isoprenaline-induced cardiac toxicity by stabilizing cardiac marker enzymes and membrane-bound ATPases

Intake of tea flavonoids has been reported to reduce the incidence of cardiovascular disease. The present study was undertaken to investigate the preventive effect of (-)epigallocatechin gallate (EGCG) on heart weight, cardiac marker enzymes, membrane-bound ATPases and electrolytes in isoprenaline (ISO)-induced myocardial infarcted (MI) Wistar rats. Rats subcutaneously administered ISO 100 mgkg(-1) at intervals of 24 h for 2 days resulted in significant increases in heart weight and the activities of cardiac marker enzymes such as creatine kinase, creatine kinase-MB, lactate dehydrogenase (LDH), aspartate transaminase and alanine transaminase in serum, and significant decreases in the activities of these enzymes in the myocardium. ISO injection also increased levels of LDH isoenzymes (LDH 1 and LDH 2). The activity of Na+/K+ ATPase was decreased significantly and the activities of Ca2+ and Mg2+ ATPases were increased significantly in ISO-induced MI rats. Furthermore, the levels of potassium were lowered and the levels of sodium and calcium were increased in ISO-induced MI rats. Prior treatment with EGCG (10, 20 and 30 mgkg(-1)) daily for a period of 21 days reduced the effects of ISO on heart weight, activities of cardiac marker enzymes and membrane bound-ATPases and levels of LDH 1 and LDH 2 and electrolytes. Thus, EGCG exhibits beneficial effects on these enzymes and electrolytes. The observed effects may be due to the antioxidant and membrane-stabilizing effects of EGCG in ISO-induced MI rats.

Aspartate and glutamate prevents isoproterenol-induced cardiac toxicity by alleviating oxidative stress in rats

The protective effect of aspartate and glutamate in isoproterenol induced myocardial infarction (MI) was investigated in experimental animals. Male albino wistar rats were pretreated with aspartate [100 mg (kg body weight)-1day-1] or glutamate [100 mg (kg body weight)-1day-1] intraperitoneally for a period of 7 days. Following amino acid treatment, MI was induced in rats by subcutaneous injection of isoproterenol [200 mg (kg body weight)-1day-1] for 2 days. After 24 h following the last injection, the animals were sacrificed and the biochemical analysis was carried out. The activities of cardiac marker enzymes (alanine transaminase, aspartate transaminase, lactate dehydrogenase and creatine phosphokinase) were increased significantly ( P<0.05) in the serum of MI induced rats as compared to control rats. The levels of glutathione and mitochondrial ATP and the activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase and glutathione reductase) were decreased whereas lipid peroxides increased significantly ( P<0.05) in the heart of MI induced rats as compared to control rats. However, pretreatment with aspartate or glutamate to MI induced rats significantly ( P<0.05) reduced the activities of cardiac marker enzymes and increased the activities of antioxidant enzymes as compared to MI induced rats. Aspartate or glutamate pretreatment also increased the levels of glutathione and mitochondrial ATP while decreased the level of lipid peroxides in the cardiac tissue. The overall effects of aspartate and glutamate in reducing the oxidative stress in MI induced rats are similar. There was no significant difference between the control rats and aspartate or glutamate treated control rats. The present study shows that aspartate and glutamate could reduce oxidative stress in MI induced rats.

Effects of interaction of vitamin A and Rauwolfia vomitoria root bark extract on marker enzymes of cardiac diseases

Serum creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and aspartate aminotransferase (AST) are key players in the diagnostic study of cardiac complications. These enzymes are specific diagnostic markers of myocardial infarction and hypertension is a disease condition characterized with a wide range of complications, including myocardial infarction. In this study, we determined the effects of interaction of vitamin A and Rauwolfia vomitoria (RV) root bark extract on marker enzymes of cardiac diseases. CK and CK-MB activities had significant decrease in the group of animals with concomitant administration of vitamin A (40 IU/kg body wt.) and 150 mg/kg body wt. of RV root bark extract. At the interaction of vitamin A with 300 mg/kg body wt. RV root bark extract, CK-MB only showed significant (p ≥ 0.05) decrease while CK decreased insignificantly. Also at the interaction of vitamin A with 300 mg/kg body wt. RV root bark extract, AST increased significantly but decreased significantly at the interaction of vitamin A (40 IU/kg body wt.) and 150 mg/kg body wt. of RV root bark extract. Our findings showed that vitamin A dose did not lower the activities of cardiac marker enzymes. However, concomitant administration of RV root bark extract at 150 mg/kg body wt. with vitamin A shows significant reduction in the activities of CK, CK-MB and AST. These findings suggest that interaction of vitamin A with RV root bark extract would be a meaningful ethno-pharmaceutical approach in the management of myocardial infarction and treatment of hypertension.

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. The activity of creatine kinase-MB and lactate dehydrogenase were increased significantly ( P < 0.05) in the serum of isoproterenol induced cardiotoxic rats. The levels of lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides) were significantly ( P < 0.05) increased and the level of reduced glutathione was significantly ( P < 0.05) decreased in the plasma and heart of isoproterenol induced cardiotoxic rats. The activities of lysosomal enzymes (β-glucuronidase, β- N-acetylglucosaminidase, β-galactosidase, cathepsin-B and D) were increased significantly ( P < 0.05) in the serum and heart of isoproterenol induced cardiotoxic rats. Isoproterenol induction also resulted in decreased stability of membranes, which was reflected by lowered activities of β-glucuronidase and cathepsin-D in lysosomal fraction. Pretreatment with gallic acid (15 mg/kg) to isoproterenol treated rats significantly ( P < 0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes. Oral treatment with gallic acid (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study show that gallic acid prevents the lysosomal membrane damage against isoproterenol induced cardiac damage and brought back the activities of lysosomal enzymes to near normal levels. The observed effects of gallic acid are due to antilipoperoxidative and antioxidant effects.

Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats

Diets rich in natural antioxidants are associated with reduced risk of heart diseases. This study was aimed to evaluate the preventive role of naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85 mg/kg) at an interval of 24 h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (β-glucuronidase, β- N-acetyl glucosaminidase, β-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of β-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with naringin (10, 20 or 40 mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats. Thus, naringin possess cardioprotective effect in ISO-induced MI in rats.