Evaluation of Cardiomyopathic Effect of Naringin and Sinapinic Acid

Abstract

Introduction: Diabetic cardiomyopathy is the result of diabetes-induced cardiac injury, which is intimately linked to the production of oxidative stress and inflammation. Both Naringin (NA) and Sinapinic Acid (SA) have anti-inflammatory and antioxidant properties. It is unknown, nevertheless, if NG and SA can prevent diabetic cardiomyopathy by controlling inflammation and oxidative stress.

Objectives: This study used an analysis of type 1 diabetic mice induced with streptozotocin (STZ) to examine the effects of NG and SA on diabetic cardiomyopathy.

Methods: In this technique, Wistar rats each weighing 150 to 200 gm of body weight were utilized for performing the experiment. Experimental animals were segregated into five groups, each group containing six animals.  30 minutes prior to the treatment of Naringin, SA and Glibenclamide, all the experimental animals were administered with 2 g/kg of glucose substrate solution through oral route of administration. After 28th day, heart was separated from all the animals, the tissue was homogenated and then extract the supernatant liquid by employing centrifugation process. Supernatant liquid was utilized for estimating Total Creatine kinase (CK), Creatine kinase isomerize (CK-MB) and Troponin-I enzymes. These enzymes were estimated employing commercial kits (Biosystems) in semi-auto analyzer. For Histological analysis, the animal cardiac tissue was isolated and thoroughly rinsed with normal saline solution and immersed in formalin (10%). The excised specimens were then embedded in liquid paraffin and were appropriately sectioned into 5 μm thickness. The fixed myocardial sections were stained by employing eosin and Heamatoxylin.

Results: Diabetic cardiomyopathy was specifically characterized primarily by diastolic and then by systolic dysfunction along with intracellular potassium loss and calcium and sodium ions retention. STZ showed increased Total CK, Troponin-I and CK-MB when correlated with normal values. Increased levels of enzymatic biomarkers such as Total CK, Troponin-I and CK-MB was observed in STZ administered experimental rats when correlated with normal animal groups. Histopathological analysis of Naringin and SA against diabetes induced by STZ in rat myocardium was studied. STZ induced diabetes in experimental rats showed a large infarct area with predominant lymphocytic fibrosis and infiltration. Treatment with Naringin and SA dose-dependently reversed these morphological manifestations. Control group animal cardiac tissue demonstrated a regular cardiac cells arrangement.

Conclusions: Naringin at a dose of 100 and 200 mg/Kg showed significant reduction of cardiac biomarkers in STZ induced diabetes in experimental rats. SA at a dose of 150 and 300 mg/Kg showed significant reduction of cardiac biomarkers in STZ induced diabetes in experimental rats.