Isoproterenol-induced Myocardial Infarction In Rats Research Articles

Isolation and Quantification of Nanovesicles in Isoproterenol-Induced Myocardial Infarcted Rats

Introduction and Aim: Myocardial infarction (MI) is one of the leading causes of death worldwide. The pathogenesis and aetiology of MI is still unclear and there is currently no cure for MI. Cardiac troponin is the only well-known cardiac-specific marker for the diagnosis of MI but due to the delayed release of troponin in the circulation, a novel cardiac biomarker is needed in the early stages of development of MI to reduce MI mortality. Recently, it has been reported that exosome concentration is highly regulated by stress and cardiovascular diseases (CVDs). We assessed the hypothesis that exosome secretion by the injured cardiomyocytes is increased during MI and thereby serve as biomarker for MI. The aim of this study was to quantify exosomes in an isoproterenol (ISO)-induced MI rats. Method: Twelve rats were divided into two groups (group A and B). Group-A (n=6) was the normal control rats and group-B (n=6) was the ISO-treated group. Group-B animals were injected with isoproterenol (85mg/kg/bw) for two consecutive days to induce MI. Blood pressure (BP), heart rate (HR) and body weight were monitored for 7 days in all animals prior the ISO injection and throughout the experiment. After second ISO-injection, all animals were sacrificed and blood, heart tissues were obtained. Histopathological analysis was performed in heart tissue samples and levels of cardiac markers (creatine kinase-MB, lactate dehydrogenase and troponin T) were measured from the serum. Exosomes were isolated from the plasma by differential ultracentrifugation. Exosomes were quantified and characterized using nanoparticle tracking analysis (NTA), transmission electron microscope (TEM) study and ELISA for the quantification of circulating exosomal protein (CD63). Result and Discussion: ISO injection caused the development of MI and was confirmed by the increase in BP, Cardiac markers (cardiac troponin T, lactate dehydrogenase and creatine kinase). NTA together with TEM analysis revealed particle sizes of the exosome and showed an elevated number of the exosome in ISO-treated animals. Levels of exosomal protein (CD63) were also increased in ISO-treated animals. Conclusion: The concentration of exosomes was increased in MI rats indicating that circulating exosomes may be used as a novel diagnostic marker for MI.

Cardioprotective Potential of Ethanol Extract of Sonchus Arvensis L. Leaves on Isoproterenol-Induced Myocardial Infarction in Rat

Sonchus arvensis L. leaves have been used traditionally to treat various disease conditions. This study is designed to evaluate cardioprotective potential of ethanol extract of S. arvensis leaves on isoproterenol-induced myocardial infarction in Wistar rat. Male Wistar albino rats were divided into three main groups: negative control (saline only), positive control (isoproterenol only), and S. arvensis extract treated groups. S. arvensis extract was administered in three doses; 50, 100, and 200 mg/kg b.w. p.o for 14 days. On day 13 and 14, isoproterenol (85 mg/kg bw) was given intraperitoneally to positive control and extract treated groups. The parameters studied were cardiac biomarker enzymes which were Creatine Kinase (CK), Creatine Kinase-MB (CK-MB), Aspartate Transaminase (AST), Alanine Transaminase (ALT) and Lactate Dehydrogenase (LDH). The results showed that S. arvensis at dose of 50 mg/kg b.w. could significantly (P<0.05) reduce the level of CK, CK-MB, AST, ALT, and LDH in myocardial infarcted rats compared to positive control. The increase of the dose of S. arvensis extract was not followed by an increase of its cardioprotective activity. In conclusion, Sonchus arvensis L. leaves extract at dose of 50 mg/kg b.w. has potential to be developed as cardioprotective drug.

Sitagliptin prevents isoproterenol-induced myocardial infarction in rats by modulating nitric oxide synthase enzymes

Ischemic heart disease is a common cause of mortality worldwide. Sitagliptin is a new anti-diabetic drug acting as dipeptidyl peptidase-4 (DPP-4) inhibitor. The study investigated the ability of sitagliptin to prevent pathological changes of isoproterenol- (ISO-) induced myocardial injury in rats. The role of nitric oxide (NO) was also reported. Rats were assorted into six groups (n = 7) and treated for 12 days. Group 1: normal control, received normal saline. Group 2, sitagliptin control, received sitagliptin (10 mg/kg, orally). Group 3, ISO group, received isoproterenol (ISO) (100 mg/kg, i.p.). Group 4, sitagliptin + ISO, co-treated with sitagliptin plus ISO. Group 5, L-NNA + ISO, co-treated with L-NG-nitro arginine (L-NNA) (25 mg/kg, orally) plus ISO. Group 6, sitagliptin + L-NNA + ISO, co-treated with sitagliptin plus ISO plus L-NNA. Blood glucose, serum creatine kinase-MB (CK-MB, and cardiac tissue parameters of oxidative stress parameters and NO, along with histopathological examination, and immunohistochemical study of inducible NO synthase (iNOS) expression were done. The results showed that sitagliptin caused a significant reduction in CK-MB, and attenuated histopathological damage-induced by ISO. Its effect was associated with a significant decrease in oxidative stress parameters, NO contents as well as by a significant decrease in the expression of iNOS in cardiac tissue. The protective effect of sitagliptin was abrogated by coadministartion of L-NNA, a selective inhibitor of both endothelial NOS (eNOS) and neuronal NOS (nNOS). In conclusion, sitagliptin ameliorates ISO-induced myocardial injury via antioxidant effects and modulation of NOS enzymes.

Comparative Pharmacokinetics of Gallic Acid After Oral Administration of Gallic Acid Monohydrate in Normal and Isoproterenol-Induced Myocardial Infarcted Rats.

Gallic acid (GA) is a polyphenolic natural product widely distributed in food, beverage, and traditional Chinese herbs with beneficial effects on the cardiovascular system. In this research, a comparative study was conducted to investigate the possible difference of pharmacokinetic process in normal and isoproterenol-induced myocardial infarcted rats after oral administration of GA monohydrate with the dose of 50 and 100 mg/kg, respectively. Quantification of GA in rat plasma was achieved by using a simple and rapid high-performance liquid chromatographic method. The results revealed that pharmacokinetics of GA were greatly different between normal and pathological state. GA exhibited slower absorption into the bloodstream, and yielded 1.7-fold (50 mg/kg GA) and 1.3-fold (100 mg/kg GA) less values of area under concentration–time curve as well as 2.5-fold lower of maximum blood concentration (Cmax) in MI rats than those in normal rats. In addition, significant prolonged T1/2 and MRT as well as decreased CL were also registered in MI rats. Our findings suggest that myocardial infarction could alter the pharmacokinetic process of GA, and thus the potential pharmacokinetic differences of herbal preparations (or dietary nutrition) containing GA between normal and pathological conditions should be brought to the forefront seriously in clinical practice.

MYOCARDIAL POTENCY OF AQUEOUS EXTRACT OF HARUNGANA MADAGASCARIENSIS STEM BARK AGAINST ISOPROTERENOL-INDUCED MYOCARDIAL DAMAGE IN RATS

Objectives: The present study was undertaken to evaluate the effects of Harungana madagascariensis on electrocardiographical, biochemical and histopathological changes in isoproterenol (ISO)-induced myocardial infarction in rats. Methods: Male Wistar albino rats were randomly divided and treated with the aqueous extract of Harungana madagascariensis stem bark (AEHM, 200 and 400 mg/kg per os), or normal saline or vitamin E for 7 days with concomitant administration of ISO (85 mg/kg, subcutaneously) on 8th and 9th days, at 24 h interval. Results: The ISO injections to the rats caused cardiac dysfunction evidenced by a marked (P<0.01) elevation in ST-segment, a reduction in R wave amplitude (P<0.01), decrease in endogenous antioxidant reduced glutathione (GSH), increase in malondialdehyde (MDA), a lipid peroxidation marker, increase of cardiac marker enzymes lactate dehydrogenase (LDH), aspartate amino transferase (AST) and alanine amino transferase (ALT). All these changes in cardiac function as well as GSH, MDA and the enzymes (LDH, AST and ALT) were ameliorated when the rats were pretreated with AEHM. Additionally, the protective effects were strengthened by improved histopathological changes, which specify the protection of cardiomyocytes from the deleterious effects of ISO. Conclusion: This study demonstrates the cardioprotective effect of Harungana madagascariensis on isoproterenol-induced myocardial infarction in rats. The mechanism might be associated with the enhancement of antioxidant defense, reduction of lipid peroxydation and it is confirmed by amending electrocardiographic pattern, improvement of cardiac markers and less histopathological damages following ISO-induced myocardial infarction. It could provide experimental evidence to support the use of Harungana madagascariensis used in traditional medicine to treat cardiovascular disorders. Peer Review History: Received 9 February 2018; Revised 22 February; Accepted 28 February, Available online 15 March 2018 UJPR follows the most transparent and toughest ‘Advanced OPEN peer review’ system. The identity of the authors and, reviewers will be known to each other. This transparent process will help to eradicate any possible malicious/purposeful interference by any person (publishing staff, reviewer, editor, author, etc) during peer review. As a result of this unique system, all reviewers will get their due recognition and respect, once their names are published in the papers. We expect that, by publishing peer review reports with published papers, will be helpful to many authors for drafting their article according to the specifications. Auhors will remove any error of their article and they will improve their article(s) according to the previous reports displayed with published article(s). The main purpose of it is ‘to improve the quality of a candidate manuscript’. Our reviewers check the ‘strength and weakness of a manuscript honestly’. There will increase in the perfection, and transparency. Received file: Comments of reviewer(s): Average Peer review marks at initial stage: 5.5/10 Average Peer review marks at publication stage: 8.0/10 Reviewer(s) detail: Dr. Mohamed Said Fathy Al-Refaey, University of Sadat City, Menofia, Egypt, Mohamed.said@fop.usc.edu.eg Dr. Mohamed Salama, Modern University for Technology & Information, Egypt, salama47@yahoo.com Similar Articles: ANTIHYPERGLYCEMIC AND ANTI-OXIDANT POTENTIAL OF ETHANOL EXTRACT OF VITEX THYRSIFLORA LEAVES ON DIABETIC RATS STUDY ON FRESH LEAF AQUEOUS EXTR STUDY ON FRESH LEAF AQUEOUS EXTRACT OF FLACOURTIA INDICA FOR HEPATOPROTECTIVE, ANTI-ANEMIC AND HYPOGLYCEMIC ABILITIES IN CCL4 INDUCED HEPATOTOXICITY IN ALBINO WISTAR RATS

Enalapril Confers Protective Effect on Isoproterenol-Induced Myocardial Infarction in Rats through Downregulation of Cardiac Troponin, C-reactive Protein, Upregulation of IL-10β as Well as Anti-Oxidant and Anti-inflammatory Activities

Enalapril Confers Protective Effect on Isoproterenol-Induced Myocardial Infarction in Rats through Downregulation of Cardiac Troponin, C-reactive Protein, Upregulation of IL-10β as Well as Anti-Oxidant and Anti-inflammatory Activities

Chemical Composition and Ameliorative Effect of Tomato on Isoproterenol-induced Myocardial Infarction in Rats

Chemical Composition and Ameliorative Effect of Tomato on Isoproterenol-induced Myocardial Infarction in Rats

Raspberry ketone protects against isoproterenol-induced myocardial infarction in rats

AimThe cardioprotective role of raspberry ketone (RK) against isoproterenol (ISO)-induced myocardial infarction (MI) in rats was assessed. Materials and methodsRats were randomly divided into Group I - Vehicle control; Group II - Toxic control ISO (85mg/kg, s.c.); Group III, IV and V - RK (50, 100 and 200mg/kg, respectively) with ISO; Group VI- RK (200mg/kg) alone; Group VII - Propranolol (10mg/kg) with ISO; and Group VIII - Propranolol (10mg/kg) alone. After twenty-four hours of the last dose, animals were sacrificed and creatine kinase-MB, lactate dehydrogenase, total cholesterol, triglycerides, high-density-lipoprotein, low-density-lipoprotein, very-low-density-lipoprotein, malondialdehyde, reduced glutathione, superoxide dismutase, catalase, Na+, K+-ATPase, nitric oxide, histopathological and immunohistochemical analysis (tumor necrosis factor-α and inducible nitric oxide synthase) were performed. Key findingsTreatment with ISO significantly deviated the biochemical parameters from the normal levels, which were considerably restored by RK at 100 and 200mg/kg doses. 50mg/kg dose, however, did not demonstrate any significant cardioprotective action. The histopathological and immunohistochemical analysis further substantiated these findings. SignificanceOur study showed a dose-dependent reduction in oxidative stress, inflammation and dyslipidemia by RK in ISO-intoxicated rats, which signifies that RK from the European red raspberry plant might be a valuable entity for the management of MI.

Terminalia pallida fruit ethanolic extract ameliorates lipids, lipoproteins, lipid metabolism marker enzymes and paraoxonase in isoproterenol-induced myocardial infarcted rats.

The present study aimed to evaluate the effect of Terminalia pallida fruit ethanolic extract (TpFE) on lipids, lipoproteins, lipid metabolism marker enzymes and paraoxonase (PON) in isoproterenol (ISO)-induced myocardial infarcted rats. PON is an excellent serum antioxidant enzyme which involves in the protection of low density lipoprotein cholesterol (LDL-C) from the process of oxidation for the prevention of cardiovascular diseases. ISO caused a significant increase in the concentration of total cholesterol, triglycerides, LDL-C, very low density lipoprotein cholesterol and lipid peroxidation whereas significant decrease in the concentration of high density lipoprotein cholesterol. ISO administration also significantly decreased the activities of lecithin cholesterol acyl transferase, PON and lipoprotein lipase whereas significantly increased the activity of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase. Oral pretreatment of TpFE at doses 100, 300 and 500 mg/kg body weight (bw) and gallic acid (15 mg/kg bw) for 30 days challenged with concurrent injection of ISO (85 mg/kg bw) on 29th and 30th day significantly attenuated these alterations and restored the levels of lipids, lipoproteins and the activities of lipid metabolizing enzymes. Also TpFE significantly elevated the serum antioxidant enzyme PON. This is the first report revealed that pretreatment with TPFE ameliorated lipid metabolic marker enzymes and increased the antioxidant PON in ISO treated male albino Wistar rats.

Diosmin Prevents Isoproterenol-Induced Heart Mitochondrial Oxidative Stress in Rats.

Cardiac mitochondrial oxidative stress causes mitochondrial damage that plays an important role in the pathology of myocardial infarction. The preventive effects of diosmin on cardiac mitochondrial oxidative stress in isoproterenol-induced myocardial infarcted rats were evaluated. Rats were pretreated with diosmin (10mg/kg body weight) daily for 10days. Myocardial infarction was induced in rats by isoproterenol (100mg/kg body weight) injection twice at an interval of 24h (on 11th and 12th day). Isoproterenol-induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium ion, and a significant decrease in the levels of heart mitochondrial glutathione peroxidase, reduced glutathione, glutathione-S-transferase, isocitrate, malate, α-ketoglutarate, and succinate dehydrogenases. Transmission electron microscopic findings revealed damaged mitochondria with loss of cristae, swelling, and vacuolation in isoproterenol-induced rats' heart. Diosmin pretreatment showed significant preventive effects on all the biochemical parameters, and the structure of mitochondria was evaluated. Furthermore, the transmission electron microscopic study confirms the biochemical findings. The antioxidant and negative inotropic effects of diosmin inhibited cardiac mitochondrial oxidative stress and prevented mitochondrial damage in myocardial infarcted rats.

Protective effects of ethanolic peel and pulp extracts of Citrus macroptera fruit against isoproterenol-induced myocardial infarction in rats

Increases in the incidence of cardiovascular disease (CVD) have aroused strong interest in identifying antioxidants from natural sources for use in preventive medicine. Citrus macroptera (C. macroptera), commonly known as “Satkara”, is an important herbal and medicinal plant reputed for its antioxidant, nutritious and therapeutic uses. The aim of the present study was to investigate the cardio-protective effects of ethanol extracts of C. macroptera peel and pulp against isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Male albino Wistar rats (n=36) were pre-treated with peel and pulp extracts (500mg/kg) for 45days. They received a challenge with ISO (85mg/kg) on the 44th and 45th days. Our findings indicated that subcutaneous injection of ISO induced severe myocardial injuries associated with oxidative stress, as confirmed by elevated lipid peroxidation (LPO) and decreased cellular reduced glutathione (GSH) and anti-peroxidative enzymes, including glutathione peroxidase, glutathione reductase and glutathione-S-transferase, compared with levels observed in control animals. Pre-treatment with C. macroptera peel and pulp extracts prior to ISO administration however, significantly improved many of the investigated biochemical parameters, i.e., cardiac troponin I, cardiac marker enzymes, lipid profile and oxidative stress markers. The fruit peel extract showed stronger cardio-protective effects than the pulp extract. The biochemical findings were further confirmed by histopathological examinations. Overall, the increased endogenous antioxidant enzyme activity against heightened oxidative stress in the myocardium is strongly suggestive of the cardio-protective potential of C. macroptera.

Cardioprotective effect of nesfatin-1 against isoproterenol-induced myocardial infarction in rats: Role of the Akt/GSK-3β pathway

The present study was designed to evaluate the cardioprotective effects of nesfatin-1, a novel peptide with anorexigenic properties, in rats with isoproterenol (ISO)-induced myocardial infarction (MI), and to further investigate the role of Akt/GSK-3β signaling pathway in the protective effect of nesfatin-1. To induce MI, ISO was subcutaneously injected into the rats for two consecutive days at a dosage of 85mg/kg/day. ISO-induced myocardial damage was indicated by elevated levels of cardiac specific troponin-T, enhanced myocardial expression of proinflammatory cytokines (interleukin-1β, interleukin-6 and tumor necrosis factor-α), and increased number of cells with apoptotic and necrotic appearance in the myocardial tissue. Levels of p-Akt/Akt and p-GSK-3β/GSK-3β significantly decreased in heart tissue after ISO-induced MI. However, intraperitoneal administration of nesfatin-1 (10μg/kg/day) elicited a significant cardioprotective activity by lowering the levels of cardiac troponin-T and proinflammatory cytokines, indicating the protective effect of nesfatin-1 against ISO-induced MI. The biochemical findings were further confirmed by histopathological examination, which was demonstrated by reduced number of apoptotic and necrotic cells. Moreover, expressions of p-Akt/Akt and p-GSK-3β/GSK-3β in the myocardium of MI group rats were significantly increased by nesfatin-1 administration, suggesting that nesfatin-1, which appears to possess anti-apoptotic and anti-inflammatory properties, may confer protection against ISO-induced MI via an Akt/GSK-3β-dependent mechanism.

In vivo and molecular docking studies using whole extract and phytocompounds of Aegle marmelos fruit protective effects against Isoproterenol-induced Myocardial infarction in rats.

Myocardial infarction (MI) is a leading major health problem with increased morbidity and mortality worldwide. The present study investigates isoproterenol (ISO) induced MI and the beneficial role of Aegle marmelos fruit extract (AMFE) in rats. Our results indicated the significant augmentation of plasma nitric oxide (NOx) levels, C-reactive protein (CRP), homocysteine, apolipoprotein B (apo-B), cardiac tissue lipid peroxidation and liver 3-hydroxy-3 methyl glutaryl CoA (HMG-CoA) reductase activity in ISO treated rats (85mg/kg b.wt) with a concomitant decrease in plasma apolipoprotein A1 (apo-A), lipase activity, paraoxonase-1 activity and cardiac tissue taurine levels when compared with controls. However, pretreatment of ISO administered rats with AMFE (150mg/kg b.wt/day for 45 days) markedly brought the observed alterations toward near normal level indicating its protective role against MI. Further, we have extended our studies to study the interaction of important phytocompounds, marmesin, marmin, umbelliferone and impertonin, present in AMFE with key enzymes, HMG-CoA reductase, iNOS, lipoprotein lipase and paraoxonase using AutoDock4. Molecular docking analysis indicated that HMG-CoA reductase, inducible nitric oxide synthase (iNOS) and lipoprotein lipase formed a strong enzyme ligand complex with impertonin. While the marmesin showed strong interaction with paraoxonase enzyme. In conclusion, our results suggest that AMFE acts as a strong protective agent against ISO-induced MI, and the bioactive compounds are responsible for this protective action which is confirmed by molecular docking studies.

Caesalpinia sappan enhances interleukin-10 levels on isoproterenol-induced myocardial infarction in rat

Caesalpinia sappan enhances interleukin-10 levels on isoproterenol-induced myocardial infarction in rat

Modulation of ECG, Myocardial Oxidative Stress Markers and Connexion 43 Expression by Ascorbic Acid and Ferulic Acid in Isoproterenol-Induced Myocardial Infarction in Rats

Objective: To assess the effects of ferulic acid (FeA) and ascorbic acid (AS) and combination of both on ECG variables, serum cardiac enzymes (AST, LDH, CK-MB), myocardial oxidative stress markers (MDA, SOD and GSH) and connexin 43 (Cx43) expressions in isoproterenol (ISO)-induced myocardial infarction. Methods: 40 male rats were equally allocated into 5 groups, 1) Control group, 2) ISO-induced MI group (rats received ISO 150 mg/Kg ip for 2 consecutive days at 24 h intervals), 3) FeA group (rats received ISO+FeA at 20 mg/kg/day po for 6 days), 4) AS group (rats received ISO+AS at 80 mg/kg/day po for 6 days) and 5) Combined group (rats received ISO+AS+FeA in the same previous doses). Results: The ISO group showed significant increase in serum cardiac enzymes (AST, CK-MB, and LDH), myocardial MDA and myocardial histopathological damage score with significant decrease in myocardial antioxidants (SOD and GSH) and Cx43expression compared to the control group (p<0.05). ECG traces of rats of ISO-induced MI, showed ST segment elevation, prolonged QT interval, shortened RR interval and increased heart rate. A combination of FeA and AS caused more significant improvement in the studied parameters than did each agent alone. ECG changes were improved significantly in the combined treatment group only. Conclusion: A combination of FeA and AS seems to offer a greater protective effect against ISO-induced myocardial infarction. This might be due to the synergism between their antioxidant properties as well as their effects on the density and location of Cx43 in myocardium.

Does selenium improve the stem cell therapeutic effect on isoproterenol-induced myocardial infarction in rats? A histological and immunohistochemical study

BackgroundMyocardial infarction has been considered as a major cause of death in humans. Stem cells offer the potential to open a new frontier in medicine.Aim of the workThe aim of this study was to evaluate whether or not selenium improves the stem cell therapeutic effect on myocardial infarction.M

Bone marrow mononuclear cells enhance anti-inflammatory effects of pravastatin against isoproterenol-induced myocardial infarction in rats

The current study investigated the combinatorial effect of pravastatin (PRAV) and bone marrow mononuclear cells (BM-MNC) on acute myocardial infarction (AMI) induced experimentally in rats. After induction of MI, rats were given oral PRAV (20 mg/kg/day) for 28 days or a bolus intravenous injection (via lateral vein) of a total of 14 × 106 autologous BM-MNC or a combination of both. Serum brain natriuretic peptide (BNP) and histologic changes in cardiac tissues were assessed. Cardiac contents of lipid peroxides, superoxide dismutase (SOD) and inflammatory biomarkers including tumor necrosis factor (TNF)-α and interleukin (IL)-1β as well as vascular endothelial growth factor (VEGF) and nitric oxide (NO) were also measured. Combined PRAV and BM-MNC treatment significantly suppressed serum BNP. Cardiac cell apoptosis and inflammatory cell infiltration in heart tissue decreased significantly in both the PRAV and the PRAV + BM-MNC groups. Cardiac lipid peroxides along with TNFα and IL-1β levels were significantly reduced in both the PRAV and PRAV + BM-MNC hosts with an increase in SOD levels. However, the combined treatment increased cardiac NO levels and did not modify cardiac VEGF levels. The current results indicated that administration of BM-MNC improved the therapeutic efficacy of PRAV treatment by improving the morphology of infarcted hearts as well as decreasing inflammation in a host, but did not do so by inducing therapeutic angiogenesis.

Anti-inflammatory, Antithrombotic and Cardiac Remodeling Preventive Effects of Eugenol in Isoproterenol-Induced Myocardial Infarction in Wistar Rat.

This study aimed to evaluate the antithrombotic, anti-inflammatory and anti-cardiac remodeling properties of eugenol in isoproterenol-induced myocardial infarction in rats. Male Wistar rats were randomly divided into four groups, control, iso [100mg/kg body weight was injected subcutaneously into rats at an interval of 24h for 2days (6th and 7th day) to induce MI] and pretreated animals with clopidogrel (0.2mg/kg) and eugenol (50mg/kg) orally for 7days and intoxicated with isoproterenol (Iso+Clop) and (Iso+EG) groups. Isoproterenol-induced myocardial infarcted rats showed notable changes in the ECG pattern, increase in heart weight index, deterioration in the hemodynamic function and rise in plasma level of troponin-T, CK-MB and LDH and ALT by 316, 74, 172 and 45%, respectively, with histological myocardium necrosis and cells inflammatory infiltration. In addition, significant increases in plasma levels of inflammatory biomarkers such as fibrinogen, α1, α2, β1, β2 and γ globulins with decrease level of albumin were observed in infarcted rats as compared to normal ones. Else, the angiotensin-converting enzyme (ACE) activity in plasma, kidney and heart of the isoproterenol-induced rats was significantly increased by 34, 47 and 93%, respectively, as compared to normal group. However, the administration of eugenol induced a clear improvement in cardiac biomarkers injury, reduced inflammatory mediators proteins, increased heart activities of superoxide dismutase and glutathione peroxidase with reduce in thiobarbituric acid-reactive substances content and inhibition of ventricular remodeling process through inhibition of ACE activity. Overall, eugenol evidences high preventive effects from cardiac remodeling process.

Cardioprotective effect of linseed oil against isoproterenol-induced myocardial infarction in Wistar rats: a biochemical and electrocardiographic study.

The present study was designed to evaluate the cardioprotective effect of Tunisian flaxseed oil (Linum usitatissimum) against isoproterenol-induced myocardial infarction in rats by studying hypertensive and cardiac damage markers especially electrocardiographic changes and troponin T serum level. In vitro, the extracted oil showed an important inhibition of angiotensin converting enzyme (ACE) with an IC50 = 85.96μg/ml. According to chemical analysis, this extract is composed essentially of alpha linolenic acid (ALA), an n-3 polyunsaturated fatty acid (58.59%). Male rats were randomly divided into three groups, namely control (C), isoproterenol (ISO), and isoproterenol-treated group with flaxseed oil (FO + ISO). Isoproterenol injection showed changes in ECG pattern, including ST-segment elevation (diagnostic of myocardial infarction), increase in the serum levels of Troponin T and cardiac injury markers (creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT)). However, Linum oil pre-co-treatment prevented almost all the parameters isoproterenol-induced myocardial infarction in rats. Results of the present study proved that flaxseed oil has a significant effect by heart protection against isoproterenol-induced myocardial infarction through beneficial effect of the important fraction of ALA.

Protective effects of Centella asiatica against isoproterenol-induced myocardial infarction in rats: biochemical, mitochondrial and histological findings

Myocardial infarction (MI) induced by isoproterenol (ISO) is a standardized model to study the beneficial effects of different drugs. The protective effect of Centella asiatica on ISO-induced cardiotoxicity and the antioxidant activity involved in the protection were investigated in rats. Wistar albino rats were used in the present study. Animals were randomly divided into six groups comprising of six animals in each group. MI was induced in rats with ISO (85 mg/kg, sc) twice at an interval of 24 hrs. ISO produced significant alterations in the creatine kinase, biochemical parameters and moderate necrosis in the heart. The effect of Centella asiatica oral treatment for 21 days at two doses (100 mg and 200 mg/kg, body weight) was evaluated against ISO -induced cardiac necrosis. Levels of marker enzymes (LDH and CK) were assessed in serum while antioxidant parameters viz., reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malondialdehde (MDA) were assayed in heart homogenate. Significant myocardial necrosis, depletion of endogenous antioxidants and increase in serum levels of marker enzymes were observed in ISO-treated animals as compared with the normal control animals. Centella asiatica showed a significant cardioprotective activity by lowering the levels of serum marker enzymes and lipid peroxidation as well as elevated the levels of antioxidant enzymes. The findings of the present study demonstrated that the cardioprotective effects of Centella asiatica on ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidants and inhibition of lipid peroxidation of membrane.