Journal of Pharmacy Research Vol.5 Issue 2.February 2012 Palanivel Karthika et al. / Journal of Pharmacy Research 2012,5(2),915-918 915-918 Research Article ISSN: 0974-6943 Available online through http://jprsolutions.info * Corresponding author. Dr. M. Rajadurai, Assistant Professor, Department of Biochemistry, Muthayammal College of Arts & Science, Rasipuram- 637408, Namakkal, Tamil Nadu, India I NTRODUCTI ON Preventive effect of esculetin on lipid peroxides and antioxidants in isoproterenol-induced myocardial infarction in Wistar rats Palanivel Karthika, Murugan Rajadurai *, Palanisamy Ganapathy, Ganesan Kanchana. Department of Biochemistry, Muthayammal College of Arts & Science, Rasipuram - 637 408, Tamil Nadu, India. Received on:10-11-2011; Revised on: 15-12-2011; Accepted on:12-01-2012 ABSTRACT The present study is undertaken to evaluate the effect of esculetin on the levels of lipid peroxidation and antioxidants in isoproterenol (ISO)-induced myocardial infarction (MI) in Wistar rats. The rats were subcutaneously injected with isoproterenol (ISO) (85 mg/kg) at an interval of 24 hours for two days. A significant increased in the levels of thiobarbituric acid reactive substances (TBARS) and hydroperoxide (HP), whereas the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione peroxidase (GPx) and non-enzymatic antioxidants like reduced glutathione (GSH), vitamin E & C were significantly decreased. Oral pretreatment with esculetin (10 and 20 mg/kg) to ISO- induced rats daily for a period of 21 days significantly decreased the levels of TBARS and HP also increased the levels of both enzymatic and non- enzymatic antioxidant. This could be due to free radical scavenging and antioxidant property of esculetin. Thus, our finding demonstrates that esculetin prevents the alterations in lipid peroxidation and antioxidants status during ISO-induced MI in rats. Key words: Esculetin; isoproterenol; myocardial infarction; lipid peroxidation; antioxidants. Cardiovascular disease (CVD) is the class of diseases that involves the heart or blood vessels. Myocardial infarction (MI) is the condition of necrosis of the heart that occurs due to imbalance between coronary blood supply and myocardial demand [2]. The responds with an increase in muscle mass and this process of hypertrophy represents a fundamental compensatory mecha- nism that permits the ventricle to sustain normal perfusion pressure [3]. Early reperfusion is the best way to reduce the progression of myocardial damage induced by ischemia reperfusion injury [4]. There is extensive evi- dence to implicate free radicals in the development of degenerative diseases [5]. Oxidative stress resulting from increased production of free radicals associ- ated with decreased antioxidants in the myocardium, play a major role in CVD such as ischemic heart disease, atherosclerosis, congestive heart fail- ure, cardiomyopathy and arrhythmias [6], which are together with other derivatives of oxygen they are inevitable by products of biological redox reactions [7]. Free radicals are continuously produced by the body’s normal use of oxygen such as respiration and some cell mediated immune functions. Reactive oxygen species (ROS) such as superoxide anions (O· - ), hydroxyl radicals (·OH) and nitric oxide (NO). The increased production of toxic oxygen derivatives is considered to be a universal feature of stress condi- tions [8]. Continuous raise in the cellular reduction potential or decrease in the redox capacity of the redox couples leads to the production of ROS, causing an imbalance in the cell ability to detoxify their toxicity and repair the damage resulting in the oxidative stress [9]. Isoproterenol (ISO), a ß-adrenoceptor agonist that is used to induce MI experimentally in rats. The infarction induced by ISO, which arises from a physiological imbalance between free radical production and the cardiac antioxidative defense system of experimental animals, is similar to that observed in human MI [10]. It is also well known to generate free radicals and to stimulate lipid peroxidation, which may be a causative factor for irreversible damage to the myocardial membrane [11]. Loss of function and integrity of myocardial membranes are the outcomes of ISO-induced myo- cardial injury involving change in membrane permeability alterations [12]. Antioxidants are beneficial components that neutralize free radicals before they can attack cells and hence prevent damage to cellular proteins, lipids and and carbohydrates. A wide range of antioxidants both natural and synthetic has been proposed for the treatment of human disease. Antioxidant action includes free radical scavenging capacity, inhibition of lipid peroxidation, metal ion chelating ability and reducing capacity [13]. Coumarins are widely distributed in plants and are especially abundant in the bark, leaves and roots of umbeilliferae and rutaceae plants, so far more than 1300 types of coumarins have been identified as natural or synthesized compounds [14]. Coumarins comprise a group of natural compounds that have recently at- tracted much attention because of their bread biological activites [15]. Esculetin (6, 7 dihydroxy coumarin) is known to be a 5 and 12-lipogenase inhibitor and to inhibit the production of leukotrienes and 5- hydroxyeicosateraenoic acid through the lipogenase pathway [16]. Escule- tin also scavenges hydroxyl radicals and inhibits lipid peroxidation in rat liver [17]. In view of the above facts, the present study was designed to evaluate the preventive effect of esculetin on the lipid peroxidases and antioxidants in ISO-induced MI in rats. MATERIALS AND METHODS Experimental animals All the experiments were done with male albino Wistar rats weighing 140- 160 g, obtained from the Venkateswara Enterprises, Bangalore were used in this study. They were housed in polypropylene cages (47x34x20 cm) lined with husk, renewed every 24 h under a 12:12 h light/dark cycle at around 22°C and had free access to tap water and food. The rats were fed on a standard pellet diet (Pranav Agro Industries Ltd., Maharashtra, India). The pellet diet consisted of 22.02% crude protein, 4.25% crude oil, 3.02% crude fiber, 7.5% ash, 1.38% sand silica, 0.8% calcium, 0.6% phosphorus, 2.46% glucose, 1.8% vitamins, and 56.17% carbohydrates. It provided a metabo- lizable energy of 3600 kcal. The experiment was carried out according to the guidelines of the Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), New Delhi, India.