Investigation of possible cardiac side effects of diclofenac in exercise-treated rats. Tasgin Erdal * , Lok Sefa Sports Sciences Faculty, Selcuk University, Campus, Konya, Turkey Abstract In this study, it was aimed to determine the effect of diclofenac administration on serum cardiac damage markers in exercised and non-exercised rats. In the study, 28 rats were divided into 4 equal groups. No application was made to control group, while the rats in the exercise group were floated for 30 min in a day. Diclofenac group were received at the dose of 13.5 mg/kg (intraperitoneally) diclofenac once a day, whereas the rats in the Diclofenac+Exercise group were floated for 30 min after than 1 h of administration of diclofenac at the dose of 13.5 mg/kg (intraperitoneally) once a day. At the end of one week, blood samples were taken from by cardiac puncture under general anesthesia and afterwards, rats are immediately euthanized. Rat-specific cardiac troponin I, creatine kinase-MB, lactate dehydrogenase, aspartate aminotransferase, alkaline phosphatase, gamma glutamyltransferase, blood urea nitrogen and creatinine levels were determined in the samples. Cardiac troponin I, lactate dehydrogenase and aspartate aminotransferase levels of Diclofenac group were statistically significantly higher (P<0.05) than the all other groups, however, statistically significant (P<0.05) fluctuations were in the creatinine levels in the experimental groups. In conclusion, it is stated that the diclofenac application may cause heart damage and diclofenac may not increase heart damage when exercised together with ingestion. Keywords: Diclofenac, Exercise, Cardiac damage. Accepted on August 18, 2017 Introduction Non-steroidal Anti-Inflammatory Drug (NSAID) has anti- inflammatory, antipyretic, and analgesic effects, and these effects of NSAIDs are explained by the inhibition of prostaglandins via inhibiting of Cyclooxygenase Enzymes (COX). COX is mainly divided into two forms as COX1 and COX2. COX-1 plays role in the normal physiological functions, whereas COX-2 may intensely increase in the tissue damage or inflammatory situations. NSAIDs have different selective inhibitory effects on the COX2/COX1. Selective effect of diclofenac on the COX2/COX1 is 4/1 [1]. Diclofenac has the most prescribed NSAIDs in the human and veterinary medicine because of its potent anti-inflammatory, antipyretic and analgesic effect when compared to other NSAIDs [2-4]. Oral, topical and parenteral formulations of diclofenac is exist and is extensively used for treatment of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, and mild to moderate pain. Diclofenac has the most inhibitor effect of prostaglandin E2 production other than NSAIDs, and this inhibitor effect of diclofenac may be over 3 to 1000 times when compared to other NSAIDs [1,5]. NSAIDs are the most widely prescribed drugs in the world, they are usually used in sports medicine, as well [6,7]. Cardiac safety of the NSAIDs is still highly debated [4,6]. Although selective COX-2 inhibitor NSAIDs has low gastrointestinal side effects, it has been clearly observed that increased usage of COX-2 is associated with myocardial infarction and stroke [1]. NSAIDs caused imbalance between COX-1 and COX-2 is the reason of cardiac side effects of these drugs [3]. It is well known that diclofenac may show cardiotoxicty in human and animals [3,4]. On the other hand, cardiac response may be affected negatively by high intensity physical exercise and acute exercise may raise heart failure markers [8-10]. Troponins are considered to be specific markers of heart damage. It is considered that the levels of troponin are associated with heart cell necrosis. Troponins are part of the myocardial sarcomeric complex in the heart, and their primary task is to maintain the relationship between thick myosin and thin actin filaments. There are three different types of cardiac troponin; Troponin C, troponin T and troponin I. Troponin I inhibits actinomyosin bridge formation. The levels of cTnI increase in the myocardial injury specifically at all ages. Within 4 h after myocardial infarction an elevation is observed and remains high for about 7 d [11]. Creatine Kinase-MB (CK- MB) enzyme plays a role in cellular energy transport [12]. Creatine Kinase-MB (CK-MB) is a sub-isoenzyme of CK enzyme and defines myocardial necrosis [13]. It is considered to be one of the specific markers for determining heart damage [3]. Lactate Dehydrogenase (LDH) and Aspartate ISSN 0970-938X www.biomedres.info Biomed Res 2017 Volume 28 Issue 17 Biomedical Research 2017; 28 (17): 7675-7678 7675