Genistein prevents isoproterenol-induced cardiac hypertrophy in rats
Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducib...
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| Published in | Canadian journal of physiology and pharmacology Vol. 90; no. 8; pp. 1117 - 1125 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article Conference Proceeding |
| Language | English |
| Published |
Plattsburgh, NY
NRC Research Press
01.08.2012
National Research Council of Canada Canadian Science Publishing NRC Research Press |
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| Abstract | Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150–200 g, 10–12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)
–1
) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg
–1
, subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (
L
-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. |
|---|---|
| AbstractList | Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150-200 g, 10-12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)(-1)) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg(-1), subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities.Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150-200 g, 10-12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)(-1)) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg(-1), subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150-200 g, 10-12 weeks old) rats. Isoproterenol (5 mg x [(kg body weight).sup.-1]) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg x [kg.sup.-1], subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150-200 g, 10-12 weeks old) rats. Isoproterenol (5 mg x [(kg body weight).sup.-1]) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg x [kg.sup.-1], subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. Key words: genistein, nitric oxide, NOS inhibitor, cardiac hypertrophy, oxidative stress, fibrosis, myocyte size. La genisteine, une isoflavone abondante dans le soya, possede d'importants effets regulateurs de la synthese d'oxyde nitrique (NO) et du stress oxydant. La liberation transitoire et faible de NO par la monoxyde d'azote synthase endotheliale (eNOS) s'est averee benefique, alors qu'une liberation elevee et soutenue par la monoxyde d'azote synthase inductible (iNOS) peut etre nefaste dans le cas d'hypertrophie cardiaque pathologique. La presente etude a ete concue pour evaluer si la genisteine pouvait prevenir l'hypertrophie cardiaque induite par l'isoproterenol chez les rats Wistar males (150-200 g ages de 10 a 12 semaines). L'isoproterenol (5 mg x [(kg body weight).sup.-1]) a ete injecte par voie sous-cutanee une fois par jour pendant 14 jours afin d'induire l'hypertrophie cardiaque. La genisteine (0,1 et 0,2 mg x [kg.sup.-1], injection sous-cutanee une fois par jour) a ete administree parallelement a l'isoproterenol. La taille des myocytes et la fibrose du tissu cardiaque ont ete etudies. Les niveaux de substances reactives acide thiobarbiturique (TBARS), de glutathion (GSH), de la superoxyde dismutase (SOD), de catalase et de 1-OH proline (contenu en collagene) ont aussi ete estimes. La genisteine prevenait significativement l'augmentation induite par l'isoproterenol du rapport du poids du coeur sur le poids corporel, de la masse ventricule gauche (echocardiographie), de la 1-OH-proline, de la fibrose, de la taille des myocytes et du stress oxydant du myocarde. Ces effets benefiques de la genisteine etaient bloques par un inhibiteur non selectif de NOS (L-NAME), contrairement a un inhibiteur selectif de iNOS (amoniguanidine). Ainsi, l'etude presente suggere que les effets salutaires de la genisteine sur l'hypertrophie cardiaque induite par l'isoproterenol peuvent faire intervenir l'inhibition de iNOS et la potentialisation des activites de eNOS. Mots-cles : genisteine, oxyde nitrique, inhibiteur de NOS, hypertrophie cardiaque, stress oxydant, fibrose, taille des myocytes. [Traduit par la Redaction] Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150–200 g, 10–12 weeks old) rats. Isoproterenol (5 mg·(kg body weight) –1 ) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg –1 , subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor ( L -NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150-200 g, 10-12 weeks old) rats. Isoproterenol (5 mg·(kg body weight)(-1)) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg(-1), subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. Genistein, an isoflavone and a rich constituent of soy, possesses important regulatory effects on nitric oxide (NO) synthesis and oxidative stress. Transient and low release of NO by endothelial nitric oxide synthase (eNOS) has been shown to be beneficial, while high and sustained release by inducible nitric oxide synthase (iNOS) may be detrimental in pathological cardiac hypertrophy. The present study was designed to evaluate whether genistein could prevent isoproterenol-induced cardiac hypertrophy in male Wistar rats (150–200 g, 10–12 weeks old) rats. Isoproterenol (5 mg·(kg body weight) –1 ) was injected subcutaneously once daily for 14 days to induced cardiac hypertrophy. Genistein (0.1 and 0.2 mg·kg –1 , subcutaneous injection once daily) was administered along with isoproterenol. Heart tissue was studied for myocyte size and fibrosis. Myocardial thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase levels, and 1-OH proline (collagen content) were also estimated. Genistein significantly prevented any isoproterenol-induced increase in heart weight to body weight ratio, left ventricular mass (echocardiographic), myocardial 1-OH proline, fibrosis, myocyte size and myocardial oxidative stress. These beneficial effects of genistein were blocked by a nonselective NOS inhibitor (L-NAME), but not by a selective iNOS inhibitor (aminoguanidine). Thus, the present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities. |
| Abstract_FL | La génistéine, une isoflavone abondante dans le soya, possède d’importants effets régulateurs de la synthèse d’oxyde nitrique (NO) et du stress oxydant. La libération transitoire et faible de NO par la monoxyde d’azote synthase endothéliale (eNOS) s’est avérée bénéfique, alors qu’une libération élevée et soutenue par la monoxyde d’azote synthase inductible (iNOS) peut être néfaste dans le cas d’hypertrophie cardiaque pathologique. La présente étude a été conçue pour évaluer si la génistéine pouvait prévenir l’hypertrophie cardiaque induite par l’isoprotérénol chez les rats Wistar mâles (150–200 g agés de 10 à 12 semaines). L’isoprotérénol (5 mg·(kg de poids corporel)
–1
) a été injecté par voie sous-cutanée une fois par jour pendant 14 jours afin d’induire l’hypertrophie cardiaque. La génistéine (0,1 et 0,2 mg·kg
–1
, injection sous-cutanée une fois par jour) a été administrée parallèlement à l’isoprotérénol. La taille des myocytes et la fibrose du tissu cardiaque ont été étudiés. Les niveaux de substances réactives acide thiobarbiturique (TBARS), de glutathion (GSH), de la superoxyde dismutase (SOD), de catalase et de 1-OH proline (contenu en collagène) ont aussi été estimés. La génistéine prévenait significativement l’augmentation induite par l’isoprotérénol du rapport du poids du cœur sur le poids corporel, de la masse ventricule gauche (échocardiographie), de la 1-OH-proline, de la fibrose, de la taille des myocytes et du stress oxydant du myocarde. Ces effets bénéfiques de la génistéine étaient bloqués par un inhibiteur non sélectif de NOS (
L
-NAME), contrairement à un inhibiteur sélectif de iNOS (amoniguanidine). Ainsi, l’étude présente suggère que les effets salutaires de la génistéine sur l’hypertrophie cardiaque induite par l’isoprotérénol peuvent faire intervenir l’inhibition de iNOS et la potentialisation des activités de eNOS. |
| Audience | Academic |
| Author | Seth, Sandeep Dinda, Amit Kumar Maulik, Subir Kumar Prabhakar, Pankaj |
| Author_xml | – sequence: 1 givenname: Subir Kumar surname: Maulik fullname: Maulik, Subir Kumar organization: Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 2 givenname: Pankaj surname: Prabhakar fullname: Prabhakar, Pankaj organization: Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 3 givenname: Amit Kumar surname: Dinda fullname: Dinda, Amit Kumar organization: Department of Pathology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 4 givenname: Sandeep surname: Seth fullname: Seth, Sandeep organization: Department of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India |
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| Keywords | Hypertrophied heart Oxidative stress Agonist Isoprenaline Rat Rodentia β2-Adrenergic receptor β-Adrenergic receptor agonist β-Adrenergic receptor Myocyte Vertebrata Mammalia Fibrosis Inhibitor |
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| PublicationYear | 2012 |
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| SubjectTerms | Animals Biological and medical sciences Biosynthesis cardiac hypertrophy Cardiomegaly - chemically induced Cardiomegaly - drug therapy Cardiomegaly - metabolism Cardiomegaly - pathology Cardiomegaly - prevention & control Cardiotonic Agents - antagonists & inhibitors Cardiotonic Agents - pharmacology Cardiotonic Agents - therapeutic use Cardiovascular disease Cardiovascular system Catalase - metabolism Cellular signal transduction Chemical compounds Disease Models, Animal Enzyme Inhibitors - pharmacology fibrose Fibrosis Fundamental and applied biological sciences. Psychology genistein Genistein - antagonists & inhibitors Genistein - pharmacology Genistein - therapeutic use Glutathione - metabolism Guanidines - pharmacology génistéine Health aspects Hydroxyproline - metabolism hypertrophie cardiaque inhibiteur de NOS Isoflavones Isoproterenol - antagonists & inhibitors Male Myocardium - metabolism Myocardium - pathology myocyte size NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide NOS inhibitor oxidative stress oxyde nitrique Pharmacology Rats Rats, Wistar stress oxydant Studies Superoxide Dismutase - metabolism taille des myocytes Thiobarbituric Acid Reactive Substances - metabolism Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| Title | Genistein prevents isoproterenol-induced cardiac hypertrophy in rats |
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