Protective effect of ursolic acid against myocardial ischemia induced by isoproterenol in rats

Senthil Selvaraj, M. Sridevi, K. V. Pugalendi

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Sustained high levels of circulating catecholamines may induce cardiotoxicity through oxidative mechanisms. Isoproterenol is a synthetic catecholamine with increasing attention owing to this application in cardiology. The aim of the present study was to investigate the cardioprotective effects of ursolic acid against isoproterenol-induced myocardial ischemia. Normal Wistar strain rats were pretreated with UA (20, 40, and 60 mg/kg, s.c.) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, s.c. for 2 consecutive days). Hearts were excised from the experimental animals and assessed for the activities of cardiac markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HPs), and conjugated dienes (CDs)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFAs), and phospholipids (PLs)], and membrane-bound enzymes (total ATPase, Na +K+ATPase, Ca2+ATPase, and Mg 2ATPase). In ISO-treated group, shrinkage of cardiac markers and elevated lipid peroxidation with compromised lipid profiles in the heart where accompanied by the decreased activities of membrane-bound enzymes. The prior administration of UA significantly (p < 0.05) prevented the isoproterenol-induced alterations and restored the enzymes to near normal. These findings indicate the cardioprotective activities of UA during isoproterenol-induced myocardial ischemia.

Original languageEnglish
Pages (from-to)57-65
Number of pages9
JournalToxicology Mechanisms and Methods
Volume17
Issue number1
DOIs
Publication statusPublished - 1 Dec 2006
Externally publishedYes

Fingerprint

Isoproterenol
Myocardial Ischemia
Rats
Lipid Peroxides
Lipids
Catecholamines
Enzymes
Cholesterol
Membranes
Cardiology
Calcium-Transporting ATPases
Thiobarbituric Acid Reactive Substances
Cholesterol Esters
Creatine Kinase
Aspartate Aminotransferases
Alanine Transaminase
L-Lactate Dehydrogenase
Nonesterified Fatty Acids
Lipid Peroxidation
Peroxidase

Keywords

  • Antioxidant Enzymes
  • Cardiac Markers
  • Lipid Peroxidation
  • Myocardial Ischemia
  • Ursolic Acid

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Protective effect of ursolic acid against myocardial ischemia induced by isoproterenol in rats. / Selvaraj, Senthil; Sridevi, M.; Pugalendi, K. V.

In: Toxicology Mechanisms and Methods, Vol. 17, No. 1, 01.12.2006, p. 57-65.

Research output: Contribution to journalArticle

@article{439fe7d1d0ff44d0b16af9e522e5fd6a,
title = "Protective effect of ursolic acid against myocardial ischemia induced by isoproterenol in rats",
abstract = "Sustained high levels of circulating catecholamines may induce cardiotoxicity through oxidative mechanisms. Isoproterenol is a synthetic catecholamine with increasing attention owing to this application in cardiology. The aim of the present study was to investigate the cardioprotective effects of ursolic acid against isoproterenol-induced myocardial ischemia. Normal Wistar strain rats were pretreated with UA (20, 40, and 60 mg/kg, s.c.) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, s.c. for 2 consecutive days). Hearts were excised from the experimental animals and assessed for the activities of cardiac markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HPs), and conjugated dienes (CDs)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFAs), and phospholipids (PLs)], and membrane-bound enzymes (total ATPase, Na +K+ATPase, Ca2+ATPase, and Mg 2ATPase). In ISO-treated group, shrinkage of cardiac markers and elevated lipid peroxidation with compromised lipid profiles in the heart where accompanied by the decreased activities of membrane-bound enzymes. The prior administration of UA significantly (p < 0.05) prevented the isoproterenol-induced alterations and restored the enzymes to near normal. These findings indicate the cardioprotective activities of UA during isoproterenol-induced myocardial ischemia.",
keywords = "Antioxidant Enzymes, Cardiac Markers, Lipid Peroxidation, Myocardial Ischemia, Ursolic Acid",
author = "Senthil Selvaraj and M. Sridevi and Pugalendi, {K. V.}",
year = "2006",
month = "12",
day = "1",
doi = "10.1080/15376510600822649",
language = "English",
volume = "17",
pages = "57--65",
journal = "Toxicology Mechanisms and Methods",
issn = "1537-6516",
publisher = "Informa Healthcare",
number = "1",

}

TY - JOUR

T1 - Protective effect of ursolic acid against myocardial ischemia induced by isoproterenol in rats

AU - Selvaraj, Senthil

AU - Sridevi, M.

AU - Pugalendi, K. V.

PY - 2006/12/1

Y1 - 2006/12/1

N2 - Sustained high levels of circulating catecholamines may induce cardiotoxicity through oxidative mechanisms. Isoproterenol is a synthetic catecholamine with increasing attention owing to this application in cardiology. The aim of the present study was to investigate the cardioprotective effects of ursolic acid against isoproterenol-induced myocardial ischemia. Normal Wistar strain rats were pretreated with UA (20, 40, and 60 mg/kg, s.c.) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, s.c. for 2 consecutive days). Hearts were excised from the experimental animals and assessed for the activities of cardiac markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HPs), and conjugated dienes (CDs)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFAs), and phospholipids (PLs)], and membrane-bound enzymes (total ATPase, Na +K+ATPase, Ca2+ATPase, and Mg 2ATPase). In ISO-treated group, shrinkage of cardiac markers and elevated lipid peroxidation with compromised lipid profiles in the heart where accompanied by the decreased activities of membrane-bound enzymes. The prior administration of UA significantly (p < 0.05) prevented the isoproterenol-induced alterations and restored the enzymes to near normal. These findings indicate the cardioprotective activities of UA during isoproterenol-induced myocardial ischemia.

AB - Sustained high levels of circulating catecholamines may induce cardiotoxicity through oxidative mechanisms. Isoproterenol is a synthetic catecholamine with increasing attention owing to this application in cardiology. The aim of the present study was to investigate the cardioprotective effects of ursolic acid against isoproterenol-induced myocardial ischemia. Normal Wistar strain rats were pretreated with UA (20, 40, and 60 mg/kg, s.c.) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, s.c. for 2 consecutive days). Hearts were excised from the experimental animals and assessed for the activities of cardiac markers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HPs), and conjugated dienes (CDs)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFAs), and phospholipids (PLs)], and membrane-bound enzymes (total ATPase, Na +K+ATPase, Ca2+ATPase, and Mg 2ATPase). In ISO-treated group, shrinkage of cardiac markers and elevated lipid peroxidation with compromised lipid profiles in the heart where accompanied by the decreased activities of membrane-bound enzymes. The prior administration of UA significantly (p < 0.05) prevented the isoproterenol-induced alterations and restored the enzymes to near normal. These findings indicate the cardioprotective activities of UA during isoproterenol-induced myocardial ischemia.

KW - Antioxidant Enzymes

KW - Cardiac Markers

KW - Lipid Peroxidation

KW - Myocardial Ischemia

KW - Ursolic Acid

UR - http://www.scopus.com/inward/record.url?scp=33845290282&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845290282&partnerID=8YFLogxK

U2 - 10.1080/15376510600822649

DO - 10.1080/15376510600822649

M3 - Article

VL - 17

SP - 57

EP - 65

JO - Toxicology Mechanisms and Methods

JF - Toxicology Mechanisms and Methods

SN - 1537-6516

IS - 1

ER -