ISO-induced Myocardial Infarction Research Articles

Protective effects of Labisia pumila var. alata on biochemical and histopathological alterations of cardiac muscle cells in isoproterenol-induced myocardial infarction rats.

The study was designed to evaluate the cardioprotective effects of the standardized aqueous and 80% ethanol extracts of Labisia pumila var. alata (LPva) in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. The extracts were administered to Wistar rats orally for 28 days with three doses (100, 200 and 400 mg/kg of body weight) prior to ISO (85 mg/kg)-induced MI in two doses on day 29 and 30. The sera and hearts were collected for biochemical and histopathological analysis after the rats were sacrificed 48 h after the first induction. The main components of the extracts, gallic acid, alkylresorcinols and flavonoids were identified and quantitatively analyzed in the extracts by using a validated reversed phase HPLC method. The extracts showed significant protective effects as pretreated rats showed a significant dose-dependent decrease (p < 0.05) in cardiac enzyme activities, i.e., cardiac troponin I (cTnI), creatine kinase MB isoenzyme (CK-MB), lactate dehydrogenase (LDH), alanine transaminase (ALT) and aspartate transaminase (AST), when compared with ISO-control rats. There were significant rises (p < 0.05) in the activity of oxidase enzymes, i.e., glutathione peroxide (GPx), catalase (CAT) and superoxide dismutase (SOD) of the pretreated rats, when compared with ISO-control group. Histopathological examination showed an improvement in membrane cell integrity in pre-treated rats compared to untreated rats. The major components of LPva extracts can be used as their biomarkers and contributed to the cardioprotective effects against ISO-induced MI rats.

Preventive Effect of Phytic Acid on Isoproterenol-Induced Cardiotoxicity in Wistar Rats

This study was aimed to evaluate the preventive role of phytic acid on membrane bound enzymes such as sodium potassium- dependent adenosine triphosphatase (Na+ /K+ ATPase), calcium-dependent adenosine triphosphatase (Ca2+ ATPase) and magnesium- dependent adenosine triphosphatase (Mg2+ ATPase) 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 phytic acid (25 and 50 mg/kg, respectively) for a period of 56 days. After the treatment period, ISO (85 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days. ISO-induced rats showed a significant decrease in the activity of Na+ /K+ ATPase and increase in the activities of Ca2+ and Mg2+ ATPase in the heart and a significant (P&lt;0.05) increase in the levels of glycoproteins in serum and the heart were also observed in ISO-induced rats. Pretreatment with phytic acid for a period of 56 days exhibited a significant (P&lt;0.05) effect and altered these biochemical parameters positively in ISO-induced rats. Thus, our study shows that phytic acid has cardioprotective role in ISO-induced MI in rats.

Preventive effect of phytic acid on lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats

This study was aimed to evaluate the preventive role of phytic acid on 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 two days showed a significant increase in the activities of lysosomal enzymes (glucuronidase, N-acetyl glucosaminidase, galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with phytic acid (25 and 50 mg/kg) daily for a period of 56 d positively altered activities of lysosomal hydrolases in ISO-induced rats. Thus, phytic acid possesses a cardioprotective effect in ISO-induced MI in rats.

Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium by Withania somnifera Leaf Extract.

We investigated the protective role of Withania somnifera leaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats.

Benidipine prevents oxidative stress, inflammatory changes and apoptosis related myofibril damage in isoproterenol-induced myocardial infarction in rats

Objective: The effects of benidipine on oxidative stress and myocardial apoptosis were assessed in isoproterenol (ISO)-induced myocardial infarction (MI) in wistar rats.Materials and method: Animals were pretreated with benidipine (1, 3, 10 μg/kg/day Body weight) intravenously for a period of 28 days. After pretreatment, ISO (85 mg/kg Body weight, subcutaneous) was injected in rats at an interval of 24 h to induce MI. Myocardial oxidative stress, cardiac biomarkers, apoptosis, inflammatory mediators, and ultrastructural architecture of the cardiac tissue were assessed in ISO-induced MI in rats.Result: Significant variation in the level of TBA, antioxidant enzymes (GSH, CAT, SOD, GPx, GRx, GST) in myocardium, cardiac biomarkers (CK-MB, LDH) in serum, Caspase-3, C-reactive protein (CRP), and alteration in ultrastructural architecture of cardiac tissue confirmed the cardiotoxicity induced by ISO. Pretreatment with benidipine preserved the lipid peroxide and antioxidant enzymes, and furthermore showed maintained levels of myocardial biomarker, CRP and caspase-3. Ultrastructure architecture of cardiac tissue was also found to be well preserved.Conclusion: The present study suggested cardioprotective effect of benidipine which may possibly be due to its antioxidant activity and antiapoptotic nature.

Beneficial role of tamoxifen in isoproterenol-induced myocardial infarction.

ER-α and ER-β agonist 17β-estradiol is reported to attenuate cardiac hypertrophy. Tamoxifen is a selective estrogen receptor modulator. Hence, the objective of this study was to investigate the effects of tamoxifen in myocardial infarction. For this, tamoxifen was administered to Sprague-Dawley rats for 1-14 days, and isoproterenol (ISO) (100 mg·(kg body mass)(-1)·day(-1)) was administered subcutaneously on the 13th and 14th days of the study in order to induce myocardial infarction, after which, various biochemical, cardiac, and morphometric parameters were evaluated. ISO produced significant dyslipidemia, hypertension, bradycardia, oxidative stress, and an increase in serum cardiac markers. Treatment with tamoxifen significantly controlled dyslipidemia, hypertension, bradycardia, oxidative stress, and reduced serum cardiac markers. The ISO control rats exhibited significant increases in the infarct size of the left ventricle (LV), LV cavity area, cardiac and LV hypertrophic indices, LV-wall thickness, cardiomyocyte diameter, and area. Treatment with tamoxifen significantly reduced infarction as well as hypertrophic and morphometric parameters. ISO also produced significant increases in the LV collagen level, decreases in Na(+)K(+) ATPase activity, and a reduction in the rate of pressure development and decay, which were prevented by tamoxifen treatment. The protective effect of tamoxifen on myocardial infarct was further confirmed by histopathological examination. Our data thus suggest that tamoxifen exerts beneficial effects in ISO-induced myocardial infarction.

Can early myocardial infarction-related deaths be diagnosed using postmortem urotensin receptor expression levels?

Myocardial infarction (MI) is one of the most prevalent causes of sudden adult death. It is difficult to diagnose early MI postmortem because there are no typical or characteristic changes in morphology. In this study, changes in the level of the mRNA for the urotensin receptor (UR) were investigated postmortem to determine the suitability of UR as a biomarker for diagnosis of early MI after death. An MI rat model was developed by injecting rats with isoproterenol (ISO) (lethal dose 850mg/kg) or normal saline (control group). The hearts of rats in the control and ISO-induced MI groups were harvested at 0, 1, 3, 6, 12, 24, 48, and 72h (h) postmortem. The hearts were then immediately submerged in 1mL of RNA stabilization solution and stored at 4°C for <1week before RNA extraction. Relative UR expression analysis was performed using the StepOne Plus Real Time PCR System with cDNA synthesized from rat heart. Postmortem UR mRNA expression was higher in the ISO-induced MI group than in the control group, at both 4 and 20°C, at all of the time points examined except 72h postmortem (p<0.0001). The largest increases were observed at ambient temperature and 6h postmortem. Based on our findings, increased postmortem UR expression could serve as a biomarker to aid diagnosis of early MI.

Metabolic pathways involved in Xin-Ke-Shu protecting against myocardial infarction in rats using ultra high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry

Xin-Ke-Shu (XKS) is a patent drug used for coronary heart diseases in China. This study evaluated the protective effect of XKS against isoproterenol (ISO)-induced myocardial infarction (MI). For its underlying mechanism in rats with MI, a metabonomic approach was developed using ultra high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC/QTOF-MS). Plasma metabolites were profiled in MI rats, pretreated orally with or without XKS. Two genres of metabolic biomarkers were used to elucidate the pharmacological action of XKS: pathological biomarkers and pharmaco biomarkers. Fifteen metabolites significantly varying between MI rats and normal rats were characterized as potential pathological biomarkers related to MI, including l-acetylcarnitine (1), l-isoleucyl-l-proline (2), tyramine (3), isobutyryl-l-carnitine (4), phytosphingosine (5), sphinganine (6), l-palmitoylcarnitine (7), lysoPC(18:0) (8), uric acid (9), l-tryptophan (10), lysoPC(18:2) (11), lysoPC(16:0) (12), docosahexaenoic acid (13), arachidonic acid (14) and linoleic acid (15). Among them, eight (1–6, 9 and 10) were first reported as pathological biomarkers related to ISO-induced MI, which mainly involved into fatty acid β-oxidation pathway, sphingolipid metabolism, proteolysis, tryptophan metabolism and purine metabolism. The metabolites significantly varying between MI rats with and without XKS pretreatment were considered as pharmaco biomarkers. A total of 17 pharmaco biomarkers were recognized, including 15 pathological biomarkers (1–15), hexanoylcarnitine (16) and tetradecanoylcarnitine (17). The results suggested that pretreatment of XKS protected metabolic perturbations in rats with MI, major via lipid pathways, amino acid metabolism and purine metabolism, which also provided a promising approach for evaluating the pharmacodynamics and mechanism of traditional Chinese medicines (TCM) formulas.

Protective role of earthworm powder (Eudrilus eugenaie) on antioxidant status and DNA fragmentation on isoproterenol-induced myocardial infarcted rats

Earthworm powder (EWP), a natural boon for medicine, has showed a wide variety of biological activities, which make it a good candidate for the treatment of many oxidative stress-mediated diseases. The present study is aimed to evaluate its therapeutic potential by estimating the levels of lipid peroxidation and assaying activities for various antioxidants in ISO-induced myocardial infarction bearing rats. Subcutaneous injection of ISO (85mg/kg body weight administered subcutaneously) to Wistar male rats for 2 consecutive days caused myocardial damage in rat heart, which was determined by the increased activity of lipid peroxidation (LPO). The heart tissue antioxidant enzymes, such as glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) and the non-enzymatic antioxidant, like reduced glutathione (GSH), vitamin C and vitamin E levels were altered in MI rats. Further, EWP (200mg/kg body weight suspended in saline) administration attenuated the antioxidant mechanism from lipid peroxidation. Thus, the modulatory effects of EWP on attenuating the lipid peroxidation, upregulation of both enzymic and non-enzymic antioxidants, and DNA fragmentation afford an assurance for the treatment of myocardial infarction in the future.

Reduction of Coenzyme Q10 Content: A Possible Effect of Isoproterenol on Heart Failure and Myocardial Infarction in Rat

Myocardial infarction (MI) was induced by subcutaneous injection of isoproterenol (ISO) to investigate the effect of ISO on Coenzyme Q10 (CoQ10) content of myocardium and subsequent effects on lipid peroxidation, electrocardiogram pattern and hemodynamic parameters of the rat's heart.36 male Wistar rats were divided randomly into 6 groups. To induce heart failure (HF) and MI, 10 and 100 mg/kg of ISO was administered subcutaneously for 10 and 2 consecutive days, respectively. The effects of ISO on myocardium CoQ10 content, concentration of malondialdehyde, ECG pattern and hemodynamic parameters of heart were analyzed.ISO-treated rats showed significant alteration in heart hemodynamic parameters such as reduction of left-ventricular systolic pressure, maximum and minimum rate of developed left ventricular pressure, besides increase of left ventricular end-diastolic pressure. Significant depletion of heart CoQ10 content (from 4.57 and 4.55 µg/100 mg tissue in control groups to 2.85 and 2.89 µg/100 mg tissue in ISO-induced HF and MI groups respectively) and increase in tissue levels of malondialdehyde (47.1 and 53.8 nmol/100 mg tissue in ISO-induced HF and MI groups, respectively) were also observed in ISO-treated animals compared with the normal animals (17.4 and 18.8 nmol/100 mg tissue in control groups, respectively). Additionally CoQ10 improved ISO effects on hemodynamic parameters and ECG pattern in ISO-induced HF and myocardial injury.The present findings have demonstrated that the cardiotoxic effects of ISO such as oxidative damage and hemodynamic declination might be related to depletion of CoQ10 concentration.

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.

Cardioprotective effect of saffron extract and safranal in isoproterenol-induced myocardial infarction in wistar rats.

This study was designed to evaluate the cardioprotective effect of Crocus sativus L. (saffron) aqueous extract and safranal, the major constituent of the essential oil of saffron, on lipid peroxidation, biochemical parameters and histopathological findings in isoproterenol (ISO)-induced myocardial infarction in Wistar rats. The saffron extract (20, 40, 80 and 160 mg/kg/day IP) or control were administered for 9 days along with ISO (85 mg/kg, SC, at 24 hr interval) on 8th and 9th day in rats. Activities of creatine kinase-muscle, brain (CK-MB) and lactate dehydrogenase (LDH) were measured using standard commercial kits. The level of malondialdehyde in heart tissue was estimated with thiobarbituric acid reactive species test. For histopathological examination, hematoxylin and eosin (H&E) staining was used. ISO administration induced a statistically significant increase (P< 0.001) in serum LDH and CK-MB and a significant increase (P< 0.001) in the levels of thiobarbituric acid reactive substances (TBARs) in the heart as compared to vehicle control rats. Saffron pretreatment (20, 40, 80 and 160 mg/kg IP) or safranal pretreatment (0.025, 0.050, 0.075 ml/kg IP) for 8 days, significantly decreased (P< 0.001) the serum LDH and CK-MB and myocardial lipid peroxidation as compared to ISO- induced rats. Histological findings of the heart sections confirmed myocardial injury with ISO administration and preserved nearly normal tissue architecture with saffron or safranal pretreatment. Saffron and safranal may have cardioprotective effect in ISO-induced myocardial infarction through modulation of oxidative stress in such a way that they maintain the redox status of the cell.

Preconditioning with diosgenin and treadmill exercise preserves the cardiac toxicity of isoproterenol in rats

This study was aimed to evaluate the preventive effect of diosgenin and exercise on tissue antioxidant status in isoproterenol-induced myocardial infarction (MI) in male Wistar rats. Levels of lipid peroxides, reduced glutathione (GSH), and the activities of glutathione-dependent antioxidant enzymes (glutathione peroxidise and glutathione reductase) and antiperoxidative enzymes (catalase and superoxide dismutase) in the plasma and the heart tissue of experimental groups of rats were determined. Pretreatment with diosgenin and exercise exerted an antioxidant effect against isoproterenol-induced myocardial infarction by blocking the induction of lipid peroxidation. A tendency to prevent the isoproterenol-induced alterations in the level of GSH, in the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. Histopathological findings of the myocardial tissue showed a protective role for combination of diosgenin and exercise in isoproterenol (ISO)-treated rats. Thus, the present study reveals that preconditioning with diosgenin and exercise exerts cardioprotective effect against ISO-induced MI due to its free radical scavenging and antioxidant effects, which maintains the tissue defense system against myocardial damage.

Effect of luteolin on lipid peroxidation and antioxidants in acute and chronic periods of isoproterenol induced myocardial infarction in rats

The present study was designed to investigate the preventive effect of luteolin on lipid peroxidation, antioxidants and histopathological findings in acute and chronic periods after isoproterenol (ISO)-induced myocardial-infarction (MI) in male Wistar rats. Luteolin supplemented by intragastric intubation at a daily dose of 0.3 mg/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 days 29 and 30th the rats of the acute MI control groups were administered 85mg/kg body weight, isoproterenol, intraperitoneally intravel of 24h. In chronic MI model luteolin administered of rat group during 30 days, and 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 significant increase in the levels of thiobarbituric acid reactive substances, lipid hydroperoxides in the heart and erythrocyte, and significant decrease in the activities of heart and erythrocytes superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione. Oral treatment with luteolin at a daily dose of (0.3 mg/kg b.wt) in both acute and chronic models showed significant decrease in the levels of heart and erythrocyte lipid peroxidation by products and significant increase in the levels of antioxidant system. The protective role of luteolin (0.3 mg/kg b.wt) on ISO-induced myocardial infarction was further confirmed by histopathological examination. Thus, the experiment clearly showed that luteolin ameliorates cardiac damage in ISO-induced myocardial infarction by prevented the accumulation of lipids due to the anti-lipid peroxidative effect.

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

This study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)-induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg/kg body weight) daily for 7 days. ISO (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce myocardial infarction (MI). Increased activity/levels of serum creatine kinase-MB (CK-MB), plasma thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes with decreased levels of plasma reduced glutathione (GSH), vitamin C, and vitamin E were observed in ISO-induced myocardial infarcted rats. Pre and cotreatment with thymol (7.5 mg/kg body weight) showed normalized activity of serum CK-MB and near normalized levels of plasma lipid peroxidation products, reduced GSH, vitamin C, and vitamin E in myocardial infarcted rats. Furthermore, the in vitro study on reducing power of thymol confirmed its potent antioxidant action. Thus, thymol protects ISO-induced MI in rats by its antilipid peroxidation and antioxidant properties.

Abstracts from the 2012 Annual Meeting of the International Society for Heart Research North American Section

Cardiovascular stress, such as that due to the synthetic catecholamine, isoprenaline (iso), can induce myocardial infarction (MI). Ethanolamine (etn) is a biogenic amine, found in certain food types, that protects the isolated rat heart against ischemiareperfusion injury. The aim of this study was to investigate the cardioprotective effects of acute etn on iso-induced MI. Male Wistar rats (250-350 g) were divided into four groups: Control (saline injections only), iso + etn (iso 67 mg/kg, s.c. and etn 10 mg/ kg i.p.), iso (67 mg/kg, s.c. and a saline injection), and etn (saline injection and 10 mg/kg i.p.). Rats were anaesthetised with sodium pentobarbitone (60 mg/kg, i.p.) and mechanically ventilated with room air. Arterial blood pressure wasmeasured from the right carotid artery and electrocardiogram (ECG) was recorded from surface leads. Infarct size was measured using triphenyltetrazolium chloride (TTC) staining and the by-products of lipid peroxidation were quantified. Iso administration significantly increased the infarct size (62.0±3.9%, Pb0.001) (mean±SEM) compared to control rats (23.7±2.7%). The heart weight/body weight (HW/BW) ratio was also significantly raised in iso rats (4.6±0.1, Pb0.001) compared to control rats (3.4±0.02). Iso + etn (5.0±0.2 Pb0.05) treated rats displayed significantly greater HW/BW ratio compared to iso treated rats. However, there was no significant difference in infarct size between iso and iso + etn. Iso + etn treated rats had a lower death rate (1.9%) compared to iso rats (11.3%). There was a significant increase in the amount of conjugated dienes (CD) in iso rats (59.56±2.6 μmol/L) compared to control rats (39.9±4.0 μmol/L, Pb0.05). There was no significant difference in the generation of CDs between control and iso + etn rats. In summary, etn seems to protect the rat from iso-induced MI; however the possibility of increased cardiac hypertrophy needs further investigation.

Amaranthus viridis Linn., a common spinach, modulates C‐reactive protein, protein profile, ceruloplasmin and glycoprotein in experimental induced myocardial infarcted rats

Glycoprotein is one of the components of the cardiac extracellular matrix and plays an important role in cardiac remodelling during various cardiac diseases, including myocardial infarction (MI). This study was aimed at evaluating the preventive role of Amaranthus viridis Linn. on C-reactive protein (CRP), total protein, albumin, globulin, ceruloplasmin and glycoproteins in the serum and heart of experimental induced myocardial infarcted (MI) rats. MI was induced in male Wistar rats by subcutaneous injection of 20 mg kg(-1) isoproterenol (ISO) kg(-1) body weight (BW) twice at an interval of 24 h. ISO-induced MI rats showed a significant increase in the levels of serum CRP and ceruloplasmin and a significant decrease in the levels of serum total protein, albumin and globulin. Glycoprotein levels in the serum and heart were increased in ISO-induced MI rats. Oral administration of 300 mg A. viridis kg(-1) BW day(-1) for a period of 45 days altered the metabolic derangement in ISO-induced MI rats. This study exemplifies the protective effect of A. viridis on ISO-induced cardiotoxicity in male Wistar rats. The data further reinforce the cardioprotective effect of A. viridis by altering CRP and glycoprotein levels.

Protective effect of morin on cardiac mitochondrial function during isoproterenol-induced myocardial infarction in male Wistar rats

Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Myocardial infarction (MI) in rats was induced by ISO (85 mg/kg) at an interval of 24 hours for 2 days. Morin was given to rats as pre-treatment for 30 days orally using an intragastric tube. ISO-treated rats showed a significant elevation of mitochondrial thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (HP) level and pre-treatment with morin significantly prevented the increase of TBARS and HP level to near normality. The level of enzymic and non-enzymic antioxidants was decreased significantly in ISO-treated rats and pre-treatment with morin significantly increased the levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and reduced glutathione to normality. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase were decreased significantly in ISO-treated myocardial ischemic rats and upon pre-treatment with morin restored these enzymes activity to normality. In addition, the decreased activities of cytochrome-C oxidase and NADH-dehydrogenases were observed in ISO-treated rats and pre-treatment with morin prevented the activities of cytochrome-C oxidase and NADH-dehydrogenase to normality. Pre-treatment with morin favorably restored the biochemical and functional parameters to near normal indicating morin to be a significant protective effect on cardiac mitochondrial function against ISO-induced MI in rats.

Preventive effect of glycosaminoglycans from Amussium pleuronectus (Linne) on biomolecules, lactate dehydrogenase-isoenzyme and electrocardiographic patterns in isoproterenol-induced myocardial infarction in Wistar rats

Objectives:This study was aimed to assess the cardioprotective role of low molecular weight glycosaminoglycans (LMW-GAG) in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Effect of LMW-GAG on biomolecules, lactate dehydrogenase (LDH)-isoenzyme, and electrocardiographic (ECG)-patterns was studied as evidence of cardioprotection.Materials and Methods:Male Wistar rats (140 ± 10 g) were divided into four groups; untreated control (group I), LMW-GAG treated (300 μg/day s. c. for 2 weeks—group II), ISO (85 mg s.c. injected on 13th and 14th days—group III), and LMW-GAG plus ISO (300 μg/day s. c. for 12 days followed by 85 mg/kg ISO on the end of 13th and 14th days—group IV). At the end of the experimental period, all animals were terminated.Results:Rats treated with LMW-GAG (300 μg/kg) for 12 days showed significant increasing levels of triglyceride (TG) (both serum and heart tissue), low density lipoprotein (LDL), very low density lipoprotein (VLDL), total cholesterol, uric acid, creatinine, and glucose. However, it significantly decreased the levels of high density lipoprotein (HDL) (serum), plasma total protein, and albumin/globulin (A/G) ratio. ISO also adversely affected the LDH-isoenzymes and caused marked elevation in ST segment. Pretreatment with LMW-GAG (300 μg/kg) daily for a period of 2 weeks prevented the ISO-treated changes.Conclusions:The results indicate that LMW-GAG exhibits a cardioprotective effect in ISO-induced MI in rats, by maintaining the biomolecules and LDH-isoenzymes.

Protective effect of Lagenaria siceraria (Mol) against membrane-bound enzyme alterations in isoproterenol-induced cardiac damage in rats

This study was aimed at evaluating the preventive role of the ethanolic extract of Lagenaria siceraria (Mol) fruit on membrane-bound enzymes, such as sodium potassium-dependent adenosine triphosphatase (Na+/K+ ATPase), calcium-dependent adenosine triphosphatase (Ca2+ ATPase) and magnesium-dependent adenosine triphosphatase (Mg2+ ATPase) on isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Male albino Wistar rats were pretreated with the ethanolic extract of L. siceraria (Mol) fruit (125, 250 and 500 mg kg−1 body weight) for a period of 30 days. After the treatment period, ISO (85mg kg−1 body weight) was subcutaneously injected into rats at 24-h intervals for 2 days. ISO-induced rats showed a significant (p < 0.05) decrease in the activity of Na+/K+ ATPase and an increase in the activities of Ca2+ and Mg2+ ATPases in the heart tissues. Pre-treatment with the ethanolic extract of L. siceraria (Mol) fruit for a period of 30 days exhibited a significant (p < 0.05) effect in ISO-induced rats. Thus, our study shows that the ethanolic extract of L. siceraria (Mol) fruit has membrane-stabilising role in ISO-induced MI in rats.