Synergistic effect of nicorandil and amlodipine on lysosomal hydrolases during experimental myocardial infarction in rats

Sathish, Venkatachalem; Ebenezar, Kesavarao Kumar; Devaki, Thiruvengadam

doi:10.1016/s0753-3322(03)00036-2

Cited by 45 publications

(34 citation statements)

References 22 publications

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“…ISO-induced myocardial necrosis involves the changes which are characterized by the loss of function and integrity of myocardial membranes. The occurrence of changes in lipid metabolism is also one of the characteristic effects of ISO [4,5]. ISO also stimulates free radical formation and lipid peroxidation, which leads to irreversible damage of the myocardial membranes [4,6].…”

Section: Introductionmentioning

confidence: 99%

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Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

Güven¹,

Sarıhan²,

Parlakpınar³

et al. 2017

Med-Science

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As aim of this study, the knowledge of whether vinpocetine (VINPO) is cardioprotective or not following isoprotenol (ISO)-induced cardiac ischemia in rats. In myocard infarction, the one of the responsible mechanisms of injury is oxidative damage and inflammmation. The effect of VINPO which is the potent antioxidant and anti inflammatory agent aimed to reveal as the biochemical, electrophysiological, and histopathologic parameters. In this study, thirty-two Wistar-Albino male rats were divided into four groups, each consisting of eight rats. The group 1 named as sham, no any drug used in this group. Group 2 named as iso group, only ISO was adminestered, the group 3 named as VINPO and iso group, here initially vinpocetine then ISO were used, and the group 4 named as iso and VINPO, here initially ISO then VINPO were used. For the rats in group 2, in first and second day ISO adminestered at a dose of 120mg/kg using an intraperitoneal injection. At third and fourth day no any drug used. And at fifth day the experiment terminated. For the rats in group 3, at the first and second day VINPO adminestered at adose of 20 mg/kg using an intraperitoneal (ip) injection, after 30 minute isoprotenol administered at adose of 120 mg/kg using an ip injection. At third and fourth day no any drug was used. And at fifth day experiment was terminated. Lastly for the rats in group4, first and second day ISO administered at a dose of 120 mg/kg using an ip injection, at third and fourth day VINPO adminestered at a dose of 20 mg/kg using an ip injection, and at fifth day experiment terminated. Prior to termination of experiment the pulse rate and ECG changes were recorded. After completion of experiment protocols blood samples and cardiac tissue samples were recieved. For the knowledge of effects of VINPO experimental miyocardial ischemia induced in rats, and the serum myoglobulin, total creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanin aminotransferase (ALT), measured. In myocardial tissue as an antioxidative system and an oxidative stres markers; malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathine (GSH), total oxidant status (TOS), total antioxidant status (TAS), oxidative stres index (OSI) were studied. As a result, VINPO showed positive impact on cardiac functions in the light of electrocardiographic, biochemical and histopathological. According to our results, it is possible to say that it exerts these beneficial effetc via its powerfull antioxidant, antiinflammatory and free radical scavenger effects.

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Section: Introductionmentioning

confidence: 99%

“…The occurrence of changes in lipid metabolism is also one of the characteristic effects of ISO [4,5]. ISO also stimulates free radical formation and lipid peroxidation, which leads to irreversible damage of the myocardial membranes [4,6]. Free oxygen radicals are reactive molecules containing an unsubstituted electron.…”

Section: Introductionmentioning

confidence: 99%

Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

Güven¹,

Sarıhan²,

Parlakpınar³

et al. 2017

Med-Science

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show abstract

“…ISO has been reported to induce infarct-like necrosis of the heart muscle (Ennis et al, 2003). It is also known to generate free radicals and to provoke lipid peroxidation leading to irreversible damage to the myocardial cell membrane (Sathish et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of CD68 after simvastatin treatment of isoproterenol‐induced myocardial infarction in rats

Atteya

2016

Int. j. adv. appl. sci.

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Isoproterenol (ISO) induces myocardial injuries in the form of ischemia and infarction (MI). Simvastatin (SIM) is a lipid-soluble inhibitor of hydroxy-3-methylglutaryl coenzyme A reductase with multiple reported therapeutic benefits. The present study was designed to evaluate the effect of pretreatment with SIM on ISO-induced cardiac infarction in rats. Forty-eight rats were divided into four groups. Group I (control) received normal saline. Group II (SIM) received SIM (10 mg/kg body weight, orally by gavage) for 30 days. Group III (ISO) received ISO (5 mg/kg) intraperitoneally for 7 days to induce cardiac injury. Group IV (ISO/SIM); received SIM (10 mg/kg body weight, orally by gavage) for 30 days and in the last 7 days they received ISO (5 mg/kg) intraperitoneally. Serological analysis for detection of cardiac injury markers (troponin-T and creatine phosphokinase-MB "CPK-MB") and inflammatory markers (IL-6 and TNF-α) was done. Cardiac tissues were processed for histological examination (H&E and Masson's trichrome) and for the immunohistological quantitative analysis of CD68. Administration of ISO induced an increase in heart weight to body weight (HW/BW) ratio and elevation of systolic and diastolic blood pressure. Serological analysis revealed an increase of interleukin-6, troponin-T, (CPK-MB), and tumor necrosis factor-α (TNF-α). Histopathological examination of heart tissue revealed thickening of the left ventricle and inter-ventricular septum, large focal areas of sub-endocardial degeneration, mononuclear cellular infiltrations, and massive interstitial fibrosis. In addition, ISO-treated rats exhibited significant up-regulation of CD68. Pre-treatment with SIM significantly attenuated ISO-induced cardiac hypertrophy and necrosis, alleviated the elevated biochemical parameters and CD68 expression, and improved the heart histopathological changes. This study provides evidence that SIM minimizes the ischemic effect of ISO on the heart of rats through inhibition of inflammatory cellular infiltration, especially macrophages, as confirmed by down-regulation of CD68.

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“…Thus, these alterations may be primary structural lesions responsible for the genesis of the process of ischemic myocardial injury. 47) A decrease in lysosomal stability is generally paralleled by increased lysosomal enzyme activity in extracellular fluid. 48) Lysosomal enzymes are important mediators of acute and chronic inflammatory diseases and involved in damage to connective tissue.…”

Section: Discussionmentioning

confidence: 99%

Protective Efficacy of Nardostachys jatamansi (Rhizomes) on Mitochondrial Respiration and Lysosomal Hydrolases during Doxorubicin Induced Myocardial Injury in Rats

Subashini

Arunachalam

Senthilkumar

et al. 2007

JOURNAL OF HEALTH SCIENCE

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Doxorubicin is highly effective in treatment for several forms of cancer. However, doxorubicin induces a cumulative and dose dependent cardiomyopathy that has been ascribed to redox-cycling of the molecule on the mitochondrial complex 1 generating in the process of increased oxidative stress. In the search of new potential cardioprotective agents, the present study is directed to explore the effect of ethanolic extract of Nardostachys jatamansi on the mitochondrial and lysosomal damage induced by doxorubicin in rats. Heart mitochondria were isolated from rats treated with doxorubicin (15 mg/kg, ip) a single dose, exhibited depressed rates of state 3 respiration, low respiratory control ratio (RCR), decreased Oxidative Phosphorylation ratio, Adenosine Triphosphate content and cytochromes (c, c 1 , b, aa 3 ). In addition the doxorubicin given rats showed significant changes in the lysosomal enzymes (Cathepsin-D, Acid phosphatase, β-D-glucoronidase, β-D-galactosidase and β-N-acetyl glucosaminidase) and membrane bound phosphatases. Also myocardial damage, as assessed by ultrastructural changes showed loss of myofibrils, mitochondrial swelling, and cytoplasmic vacuolization. Pretreatment with Nardostachys jatamansi (500 mg/kg body weight orally) for seven days ameliorated the observed abnormalities and significantly prevented the mitochondrial respiration, lysosomal integrity, membrane bound phosphatases and ultrastructural studies in doxorubicin induced rats. These findings suggest that the cardioprotective efficacy of Nardostachys jatamansi could be mediated possibly through its antioxidant effect as well as by the attenuation of the oxidative stress.

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Synergistic effect of nicorandil and amlodipine on lysosomal hydrolases during experimental myocardial infarction in rats

Cited by 45 publications

References 22 publications

Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

Down‐regulation of CD68 after simvastatin treatment of isoproterenol‐induced myocardial infarction in rats

Protective Efficacy of Nardostachys jatamansi (Rhizomes) on Mitochondrial Respiration and Lysosomal Hydrolases during Doxorubicin Induced Myocardial Injury in Rats

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