Cardiotoxicity In Wistar Rats Research Articles

Chia Seed Oil Ameliorates Doxorubicin-Induced Cardiotoxicity in Female Wistar Rats: An Electrocardiographic, Biochemical and Histopathological Approach

Doxorubicin (DOX) is a potent anti-cancer antibiotic that was widely used for treatment of various cancers. It produces free radicals which result in extreme dose-limiting cardiotoxicity. This study investigated the cardioprotective potential of chia seed oil, an active polyphenolic nutraceutical against doxorubicin-induced cardiotoxicity in Wistar rats. Twenty-four female Wistar rats were divided into four groups (n = 6) which consist of normal control, DOX control, test-A and test-B group. Animals were prophylactically treated with two different doses of test drug, i.e. chia seed oil 2.5 ml/kg/day and 5 ml/kg/day in test-A and test-B groups orally for 7 days. Doxorubicin (25 mg/kg; single dose) was administered intraperitoneally to DOX control, Test-A and Test-B animals on the seventh day to induce cardiotoxicity. ECG analysis was done before and after treatment. Besides ECG, CK, CK-MB, LDH, AST, MDA and GSH were analyzed. DOX had significantly altered ECG, CK, CK-MB, LDH, AST, MDA and GSH. Pre-treatment with chia seed oil significantly alleviated DOX-induced ECG changes and also guarded against DOX-induced rise of serum CK, CK-MB and AST levels. Chia seed oil alleviated histopathological alteration in DOX-treated rats. It also significantly inhibited DOX-induced GSH depletion and elevation of MDA. The present study revealed that chia seed oil exerts cardioprotection against doxorubicin-induced cardiotoxicity in female Wistar rats. Our study opens the perspective to clinical studies to precisely consider chia seed oil as a potential chemoprotectant nutraceutical in the combination chemotherapy with doxorubicin to limit its cardiotoxicity.

Attenuation of doxorubicin-induced cardiotoxicity in Wistar rats by aqueous leaf-extracts of Chromolaena odorata and Tridax procumbens

Ethnopharmacological relevanceChromolaena odorata (L) King and Robinson and Tridax procumbens Linn are used in traditional medicine in the treatment of diabetes mellitus and hypertension. Aim of the studyThis study investigated the potential protective role of aqueous leaf-extracts of Chromolaena odorata and Tridax procumbens against cardiotoxicity induced by doxorubicin. Materials and methodsTo this end, their impact on plasma markers of cardiac integrity, cardiac markers of oxidative stress, cardiac lipids and electrolyte profiles, and activities of cardiac ATPases, lactate dehydrogenase and creatine kinase, were monitored in doxorubicin treated rats. Metformin (250 mg/kg body weight, orally) and both extracts (50, 75 and 100 mg/kg, orally) were daily administered for 14 days; while cardiotoxicity was induced with doxorubicin (15 mg/kg, intra-peritioneally, once on the 12th day of study). ResultsThe plasma activities of creatine kinase, lactate dehydrogenase and AST of Test control were significantly (p < 0.05) higher than those of the other groups. Also, the cardiac malondialdehyde, calcium, chloride, sodium, cholesterol and triglyceride concentrations of Test control were significantly (p < 0.05) higher than those of the others. However, the cardiac concentrations of ascorbic acid, reduced glutathione, magnesium and potassium, and cardiac activities of catalase, glutathione peroxidase, superoxide dismutase, Ca2+-ATPase, Mg2+-ATPase, Na+,K+-ATPase, creatine kinase and lactate dehydrogenase of Test control were significantly (p < 0.05) lower than those of the others. ConclusionsPre-treatment with the extracts and metformin elicited a cardioprotective effect, as indicated by the prevention of doxorubicin-induced cardiac oxidative stress and prevention of adverse alterations in plasma cardiac markers, cardiac lipids and electrolyte profiles, as well as improvement of the activities of cardiac ATPases, creatine kinase and lactate dehydrogenase.

Methyl Gallate Attenuates Doxorubicin-Induced Cardiotoxicity in Rats by Suppressing Oxidative Stress

Doxorubicin-induced cardiotoxicity is the leading cause of morbidity and mortality among cancer survivors. The present study was aimed to investigate the cardioprotective potential of methyl gallate; an active polyphenolic nutraceutical, against doxorubicin-induced cardiotoxicity in Wistar rats. Twenty-four female Wistar rats (150–200 g) were divided into four groups (n = 6) which consist of normal control (group I), doxorubicin control (group II), test-A (group III), and test-B (group IV). Group III and group IV animals were prophylactically treated with methyl gallate 150 mg/kg/day and 300 mg/kg/day orally, respectively, for seven days. Doxorubicin (25 mg/kg; single dose) was administered through an intraperitoneal route to group II, III, and IV animals on the seventh day to induce acute cardiotoxicity. On the 8th day, besides ECG analysis, serum CK, CK-MB, LDH, AST, MDA, and GSH were assayed. Following gross examination of isolated hearts, histopathological evaluation was performed by light microscopy. A significant (p < 0.05) cardiac injury, as well as oxidative stress, was observed in doxorubicin control rats in comparison to normal control rats. Methyl gallate at both the doses significantly (p < 0.05) reduced doxorubicin-induced ECG changes, dyslipidaemia, and elevation of CK, CK-MB, LDH, AST, MDA and increased GSH level. Methyl gallate reversed the doxorubicin-induced histopathological changes in the heart. The present study revealed that methyl gallate exerts cardioprotection against doxorubicin-induced cardiotoxicity in female Wistar rats by suppressing oxidative stress. Our study opens the perspective to clinical studies for consideration of methyl gallate as a potential chemoprotectant nutraceutical in the combination chemotherapy with doxorubicin to limit its cardiotoxicity.

Protective Effect of Ipomoea staphylina Against Cadmium-Induced Cardiotoxicity in Wistar Rats

The present study was aimed to evaluate the protective effect of ethanolic extract of Ipomoea staphylina leaves against cadmium-induced cardiotoxicity in rats. Rats were segregated into four groups which included normal control, cadmium treated, Cd+ Ipomoea staphylina (200 mg/kg) treated, and Cd+ Ipomoea staphylina (400 mg/kg) treated. The cadmium treatment resulted in a significant increase in the activities of lactate dehydrogenase, creatine phosphokinase, serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase. Also, a significant increase in the levels of cholesterol, triglycerides, and low-density lipoprotein was noticed after cadmium treatment. On the other hand, high-density lipoprotein was significantly decreased following cadmium treatment. A significant decline in the activity of antioxidant enzymes was observed in cadmium intoxicated rats. Moreover, cadmium intoxicated rats resulted in significant increase in the levels of proinflammatory cytokines such as tumor necrosis factor alpha, interleukin 1 beta, and nitric oxide in the cardiac tissue. Supplementation of Ipomoea staphylina leaves extract to cadmium treated rats reversed most of the indices. The extract (400 mg/kg) revealed better protective effects by decreasing the activities of lactate dehydrogenase, creatine phosphokinase, serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase and improving the lipid profile. Besides, the extract also significantly improved the antioxidant enzymes activity and decreased the level of tumor necrosis factor alpha, interleukin 1 beta, and nitric oxide. Further, the histopathological study of heart supported the protective effects of Ipomoea staphylina leaves extract. The study, therefore, concludes that Ipomoea staphylina leaves extract holds a strong protective effect against cadmium-induced cardiotoxicity in rats.

Immunohistochemical and histological evaluations of cyclophosphamide-induced acute cardiotoxicity in wistar rats: The role of turmeric extract (curcuma)

Chemotherapy-induced cardiac derangement is a major concern in health sector. Cyclophosphamide as a chemotherapeutic agent induces acute cardiotoxicity through its toxic metabolite, acrolein. This study evaluated the effect of ethanol extract of turmeric on cyclophosphamide-induced acute cardiotoxicity in Wistar rats. Thirty-five healthy Wistar rats, weighing 200–250g were randomly assigned into 7 groups (Groups A, B, C, D, E, F and G) N=5. Group A was the control, group B was negative control, and group C was administered 200mg/kg of turmeric extract (orally) only. While groups B, D, E, F and G were all administered 100mg/kg cyclophosphamide (i.p) for 10 days. Groups D and E were administered 100mg/kg and 200mg/kg of turmeric extract (orally) respectively for 72 hours before cyclophosphamide administration. Groups F and G were concomitantly administered 100mg/kg cyclophosphamide (i.p) with doses of 100mg/kg and 200mg/kg of turmeric extract (orally) respectively. The rats were sacrificed under ketamine anesthesia (30mg/kg i.m). The left ventricle of the heart was excised. One-way ANOVA was used to analyze data. Results revealed that there was statistically significant (P<0.05) difference in body weight change, CK–MB, and LDH across all experimental groups; which were significantly lower in cyclophosphamide group. Histology and Immunohistochemistry revealed that there were morphological alterations in the myocardium of the left ventricle in group B while turmeric extract ameliorated cyclophosphamide-induced damage in the myocardium in other experimental groups. In conclusion, cyclophosphamide-induced myocardial alterations were significantly ameliorated through administration of ethanol extract of turmeric.

Thyme oil and thymol abrogate doxorubicin-induced nephrotoxicity and cardiotoxicity in Wistar rats via repression of oxidative stress and enhancement of antioxidant defense mechanisms

Thyme oil and thymol abrogate doxorubicin-induced nephrotoxicity and cardiotoxicity in Wistar rats via repression of oxidative stress and enhancement of antioxidant defense mechanisms

Icariin attenuates isoproterenol-induced cardiac toxicity in Wistar rats via modulating cGMP level and NF-κB signaling cascade.

Icariin, a major component of Epimedium species, was evaluated using isoproterenol (ISO)-induced cardiotoxicity in Wistar rats. Rats were treated with icariin at the doses of 1, 5, and 10 mg kg-1 orally for 15 days. Afterward, rats were administered with ISO (85 mg kg-1, subcutaneous) on 14th and 15th day to produce cardiac injury. Sildenafil (0.7 mg kg-1, intraperitoneal) was used as a positive reference to compare the effects of icariin. ISO-treated rats showed significant changes in hemodynamic parameters. Elevated levels of cardiac troponin T, nitric oxide, and tumor necrosis factor-alpha in serum, positive expression of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase in cardiac tissue, and a decrease in serum level of interleukin-10, manifested inflammation and associated cardiac injury. However, pretreatment with icariin and sildenafil significantly prevented the hemodynamic fall and showed improved contractile and lusitropic states. Furthermore, pretreatment groups also showed a reversal of other toxicity markers to normal. Additionally, pretreatment with icariin and sildenafil significantly increased the myocardial cyclic guanosine monophosphate (cGMP) levels. Our results thus indicated the potential role of icariin in the restoration of the ISO-induced cardiac toxicity and restored membrane integrity through modulation of cGMP and NF-κB signaling.

Protective effects of syringic acid, resveratrol and their combination against isoprenaline administered cardiotoxicity in wistar rats.

To evaluate the cardio-protection of syringic acid (SA) in combination with resveratrol (RV) in isoproterenol (ISO) induced myocardial infarcted (MI) rats. Groups of all rats were subjected oral pre-treatment at the beginning of the study with SA (50 mg/kg), RV (50 mg/kg) and combination (COMB) of SA (25 mg/kg) and RV (25 mg/kg) along with gallic acid (GA) (50 mg/kg) for 30 days. After sacrification, homogenate of heart tissue along with serum were utilized for further biochemical investigations. The effects on creatine kinase (CK), aspartate transaminase (AST), alanine transaminase (ALT) and gamma glutamyl transferase (GGT) were studied in serum and heart tissues. Glutathione-s-transferase (GST), glutathione peroxidase (GPX) and reduced glutathione (GSH), membrane bound enzymes and electrolytes were tested in heart tissues. Body weights and heart weights were also observed along with high sensitivity C-reactive protein (hs-CRP), uric acid and total protein content (TPC) in serum. CK, AST, ALT and GGT levels in serum were augmented significantly while these enzymes are decreased in cardiac tissue samples of ISO-treated rats. GST, GPX, GSH, Na+/K+, Mg2+, Ca2+ ATPases, K+ ions were significantly decreased while Na+ and Ca2+ ions were increased in the heart tissues of ISO-injected rats. Loss and gain of body and heart weights were noticed significantly in rats having ISO administration. ISO group showed significant increase in hs-CRP and Uric acid while significant decrease in TPC. All of actions of ISO were ameliorated by COMB. COMB suppressed ISO induced MI in rats and exhibited cardio-protection.

Modulation of doxorubicin-induced expression of the multidrug resistance gene in breast cancer cells by diltiazem and protection against cardiotoxicity in experimental animals

BackgroundDoxorubicin (DOX) is one of the most important anticancer agents used in treating breast cancer. However, chronic cardiotoxicity and multidrug resistance limit the chemotherapeutic use of DOX.MethodsThis study aimed to evaluate the capability of calcium channel blocker diltiazem (DIL) to reverse DOX resistance in breast cancer MCF-7 cells and to confer protection against DOX-induced cardiotoxicity in Wistar rats. For this purpose, we explored the effects of DOX on cell cycle phase distribution and expression of ABCB1, FOXO3a, and p53 genes in the presence and absence of DIL (20 μg/ml) and studied the ability of DIL to prevent DOX-induced cardiotoxicity after a single injection of DOX (15 mg/kg) in male Wister rats.ResultsWe found that compared with DOX alone treatment, DIL + DOX treatment down regulated the ABCB1 gene expression by > fourfold but up regulated the FOXO3a and p53 genes expression by 1.5 fold. DIL treatment conferred protection against DOX-induced cardiotoxicity, as indicated by a decrease in the levels of the cardiac enzyme creatine kinase MB and malondialdehyde and an increase in the total antioxidant capacity and glutathione peroxidase levels. These biochemical results were further confirmed by the histopathological investigation of cardiac cells, which showed normal cardiac cells with central vesicular nuclei and prevention of DOX-induced disruption of normal cardiac architecture in the DIL to DOX group.ConclusionsTaken together, our results indicate that DIL treatment can reverse the resistance of breast cancer cells to the therapeutic effects of DOX and can protect against DOX-induced cardiotoxicity in rats.

Study of Effect of Methanolic Extract of Thevetia Peruviana Leaves on Doxorubicin Induced Cardio Toxicity in Wistar Rats

Study of Effect of Methanolic Extract of Thevetia Peruviana Leaves on Doxorubicin Induced Cardio Toxicity in Wistar Rats

Subchronic dichlorvos-induced Cardiotoxicity in Wistar rats: Mitigative efficacy of Nigella sativa oil

BACKGROUND: Accidental poisoning from indiscriminate use of organophosphates have become endemic in recent decades, most especially in developing nations, coupled with the limitations of the availability of satisfactory antidotes. AIM OF THE STUDY: Thus, we investigated the cardioprotective efficacy of Nigella sativa oil (NSO) following dichlorvos dichlorvos (DDVP)-induced cardiotoxicity in Wistar rats. MATERIALS AND METHODS: A total of 24 Wistar rats were randomly divided into four groups (n = 6); the control was administered sunflower oil (1 ml/kg), DDVP (8.8 mg/kg) to the experimental Group I, whereas DDVP + NSO (8.8 mg/kg +1 ml/kg) and NSO (1 ml/kg) was administered orally to the experimental Groups II and III, respectively. The animals were euthanized; blood was transcardially collected from the right atrium, centrifuged, and plasma extracted to analyze levels of total cholesterol (TC), triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol (LDL-C). While cardiac muscle tissue was collected from the left heart, processed and stained for general architecture (hematoxylin and eosin) and elastic morphology (orcein). RESULTS: DDVP significantly (P ≤ 0.05) increased the plasma levels of TC, LDL, atherogenic and atherosclerotic indices (TC/HDL-C and LDL-C/HDL-C ratios), but this was prevented by co-administration with NSO. Histological investigations showed that DDVP resulted in the pathological appearance of cardiac tissues, such as the lack of striations, myocardial hemorrhage, and necrosis-like features. CONCLUSION: It can be concluded that NSO was able to attenuate DDVP-induced cardiotoxicity.

Kolaviron and Garcinia kola attenuate doxorubicin-induced cardiotoxicity in Wistar rats.

Background The Garcinia kola seeds have been reported for its antibacterial, antioxidant, antidiabetic and also for its chemoprevention property. The use of doxorubicin as an anticancer drug has been accompanied with avalanche of side effects including cardiotoxicity. The aim of this study was to investigate the cardioprotective effect of Kolaviron and Garcinia kola and their mechanisms of action. Methods Sixty male rats (Wistar strain) were used in this study. They were divided into 6 groups (A-F) each containing 10 animals. Group A was the control. Rats in Groups B, C, D, E and F were treated with doxorubicin at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in groups C, D, E and F were pre-treated orally with Kolaviron at the dosage of 100 mg/kg and 200 mg/kg, and Garcinia kola 100 mg/kg and 200 mg/kg for 7 days, respectively. Results The results show that doxorubicin caused a significant increase in heart rate and prolonged QT, reduced antioxidant status, increased oxidative stress, inflammation and markers of cardiac damage which were reversed by pre-treatment with Kolaviron and Garcinia kola. Conclusions Overall, pre-treatment with Kolaviron or Garcinia kola caused reversal of cardiac damage, ECG alteration and oxidative stress by increasing the activity of antioxidant enzymes and reducing the markers of inflammation on doxorubicin-induced cardiotoxicity.

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.

Cardioprotective effect of ellagic acid on doxorubicin induced cardiotoxicity in wistar rats

The objective of the study was to evaluate the cardioprotective activity of ellagic acid in doxorubicin induced cardiotoxicity. Male wistar rats (180–220 g) were divided in to four groups: vehicle control, doxorubicin control, ellagic acid (100 mg/kg) and ellagic acid (200 mg/kg). Doxorubicin was administered to all the groups except vehicle control at a dose of 3.75 mg/kg at week 2,3,4,5 to make a cumulative dose of 3.75 mg/kg. Ellagic acid was administered to the respective group of animals at a dose of 100 mg/kg 200 mg/kg, respectively once daily orally for 6 weeks. On the last day of the study, blood was collected by retro-orbital puncture and LDH and CK-MB were estimated. The animals were cannulated and the ECG and hemodynamic parameters were recorded. The animals were then sacrificed and histology of heart was performed. Doxorubicin showed cardiotoxicity manifested by changes in serum marker enzymes, ECG and hemodynamic parameters which was further confirmed by histology of heart. This doxorubicin induced changes were attenuated by treatment with ellagic acid (200 mg/kg). It has been concluded that ellagic acid (200 mg/kg) treatment for 6 weeks protects the heart of rats in doxorubicin induced cardiotoxicity.

Failure of recovery from lead‐acetate‐induced oxidative stress and cardiotoxicity in Wistar rats (648.14)

Lead poisoning continues to be a serious health problem and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being re‐settled from lead‐contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead to cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate at doses of 0.25, 0.5 and 1.0mg/ml for 6‐week duration, after which one‐half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to lead acetate produced significant decline (p&lt;0.05) in the activities of antioxidant parameters, including Glutathione peroxidase (GPx), Glutathione S‐transferase (GST), Catalase (CAT), Superoxide dismutase (SOD) and Reduced glutathione (GSH), while Malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited similar pattern of alterations, with significant (p&lt;0.05) reduction in GSH, GPx and SOD and significant elevation in MDA and H2O2 concentrations. However, GST activity was elevated, while CAT activity remained unaltered in the recovery period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters in this study failed to resolve upon withdrawal of lead exposure in male rats during the period of study.

Protective role of concomitant administration of flax lignan concentrate and omega-3-fatty acid on myocardial damage in doxorubicin-induced cardiotoxicity

The severe cardiotoxicity incurred due to doxorubicin limits the use of their therapeutic potential. The current study aims to investigate the cardioprotective effect of concomitant administration of flax lignan concentrate (FLC) and omega-3-fatty acid (ω-3-FA) on myocardial damage in doxorubicin-induced cardiotoxicity in Wistar rats. Cardiotoxicity was induced by intraperitoneal injection of doxorubicin (4mg/kg) on day 7th, 14th, 21st and 28th day in normal saline. Concomitant administration of FLC (500mg/kg) and ω-3-FA (1mL/kg) lowered TNF-α level, normalized ST, QT and mean arterial blood pressure, elevation in endogenous enzymes levels such as glutathione and lowering in malondialdehyde, super oxide dismutase followed by normalized lipid profile and reduced the mortality rate. The treatment had antiapoptotic potential at cellular level also histopathology of heart tissue (light and electron microscopical). Thus concomitant action of FLC and ω-3-FA may be antioxidant, antihyperlipidemic, anti-inflammatory and anti-apoptotic actions seem to the probable mechanisms in doxorubicin induced cardiotoxicity. It can be concluded that FLC and ω-3-FA both have distinct mechanism for cardioprotection and hence the additive effect was observed in the present study due to concomitant administration of FLC and ω-3-FA.

Cardioprotective effect of Urtica parviflora leaf extract against doxorubicin-induced cardiotoxicity in rats

AimThe present study evaluated the cardioprotective property of the hydroethanol extract of Urtica parviflora leaf material (EEUP) against doxorubicin-induced cardiotoxicity in rats. MethodsCardiotoxicity was produced by doxorubicin administration (15 mg·kg−1 i.p. for 21 days). The rats received EEUP at 200 and 400 mg·kg−1 b.w. (i.p.) daily for 21 days. After 24 h, serum cardiac biomarkers, i.e. creatine phosphokinase (CPK) and lactate dehydrogenase (LDH); serum lipid profiles, like high density lipoprotein (HDL), low density lipoprotein (LDL) and triglyceride (TG); serum biochemical parameters, viz. aspartate aminotransferase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP); myocardial antioxidant parameters, viz. malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) were measured. ResultsEEUP treatment significantly (P < 0.01) and dose dependently protected the myocardium by decreasing the elevated level of MDA; elevating the diminished levels of GSH, SOD, CAT and HDL, with a concomitant decrease in the elevated levels of HDL, LDL, and TG. EEUP also significantly (P < 0.01) reduced the increased activities of AST, ALT, ALP, CPK and LDH. The results revealed that EEUP demonstrated dose dependent cardioprotective efficacy by restoration of the serum biomarkers profile and antioxidant property. ConclusionFrom the present study, U. parviflora leaf extract showed promising cardioprotective effect against doxorubicin-induced cardiotoxicity in Wistar rats.

Efficacy of sesamol on plasma and tissue lipids in isoproterenol-induced cardiotoxicity in wistar rats

Myocardial infarction is the leading cause of death all over the world. Sesamol is a potent phenolic antioxidant contained only in processed sesame oil and possesses potent chemopreventive, antimutagenic, antihepatotoxic and antioxidation properties. This study was undertaken to investigate the effect of sesamol on plasma and tissue lipid profiles in isoproterenol (ISO) - induced rats. Myocardial infarction was induced in adult male albino rats of the Wistar strain, weighing 180-200 g, by administration of isoproterenol (85 mg/kg of body weight), subcutaneously for 2 consecutive days. Sesamol dissolved in saline (0.9% NaCl) was administered intraperitoneally once in a day in the morning for 7 days. Increased levels of total cholesterol, phospholipids, triglycerides and free fatty acids in the plasma and the decreased levels of phospholipids in tissues were observed in ISO-induced rats. Very low density lipoprotein cholesterol (VLDL-C) and low density lipoprotein cholesterol (LDL-C) increased while high density lipoprotein cholesterol (HDL-C) decreased in the plasma of ISO-induced rats. Administration of sesamol (50, 100 and 200 mg/kg of body weight) improved the above changes and brought towards normal level. The protective role of sesamol against isoproterenol-induced myocardial infarction was further confirmed by histopathological examination. These results suggest that sesamol has antihyperlipidaemic effect against cardiotoxicity.

Cardioprotective effect of Nelumbo nucifera on mitochondrial lipid peroxides, enzymes and electrolytes against isoproterenol induced cardiotoxicity in Wistar rats

ObjectiveTo explore the protective effect of Nelumbo nucifera leaf extract (NNE) on the levels of mitochondrial lipid peroxides, activities of TCA cycle and respiratory chain enzymes and electrolytes in isoproterenol (ISO) induced myocardial infarction (MI) in rats. MethodsOral pretreatment with NNE to ISO-induced rats for a period of 21 days, then heart mitochondria were isolated for the estimation of various biochemical parameters. ResultsRats induced with ISO showed significant increase in mitochondrial lipid peroxides with subsequent decrease in TCA cycle enzymes such as isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and α-ketoglutarate dehydrogenase (α-KGDH) and respiratory chain enzymes like NADH-dehydrogenase and cytochrome-c-oxidase. In addition, the levels of sodium and calcium increased and potassium decreased. Oral pretreatment with NNE to ISO-induced rats for a period of 21 days significantly reverted these biochemical parameters to near normal status. ConclusionsThus, our study suggests that NNE treatment restore energy status of the mitochondria, thereby maintaining near normal function.

Cardioprotective Activity of Methanol Extract of fruit of Trichosanthes cucumerina on Doxorubicin-induced Cardiotoxicity in Wistar Rats.

Aim and Objective:The objective was to determine the activity of methanol extract of fruit of Trichosanthes cucumerina in doxorubicin-induced cardiotoxicity in rats.Materials and Methods:The methanol extract of fruit of T. cucumerina was prepared. Male Wistar rats were divided in four groups. Group I was vehicle control. Group II animals received doxorubicin 4 mg/kg i.p. on days 21, 28, 35, and 42. Group III and IV animals were treated with methanol extract of T. cucumerina (500 and 1000 mg/kg, respectively) for 49 days. Doxorubicin was administered on days 21, 28, 35, and 42 days. The parameters of study were body weight, serum biomarkers, ECG, blood pressure, and left ventricular function. At the end of the study, the histology of heart, liver, and kidney was carried out.Results:Cardiac toxicity by doxorubicin was manifested as body weight loss, elevated serum LDH and CK-MB, increased ST, QT and QRS complex, reduced blood pressure, and left ventricular function. The methanol extract of T. cucumerina significantly decreased LDH and CK-MB, reduced ST, QT interval and QRS complex, increased heart rate, restored blood pressure, and left ventricular function. Doxorubicin caused liver and kidney necrosis, cellular infiltration, and vascular changes that indicated injury.Conclusion:T. cucumerina (1000 mg/kg) reduced the severity of doxorubicin-induced cardiac damage especially in heart. It is concluded that doxorubicin-induced cardiotoxicity is reduced by pretreatment with methanol extract of fruit of T. cucumerina.