Background: Myocardial injury due to ischemia-reperfusion (IR) is aggravated in diabetes which is associated with oxidative stress. Alleviating oxidative stress via use of antioxidants has been shown to be effective at minimizing myocardial cell death and improving cardiac function. The aim of the present study was to evaluate the cardioprotective effect of phloroglucinol against myocardial reperfusion injury (MRI) in diabetic rats.Methods: Diabetes was induced in female rats with streptozotocin (50 mg/kg). The diabetic rats were orally treated with phloroglucinol (100 and 200 mg/kg daily for 28 days). After treatment the hearts were isolated and mounted on a Langendorff apparatus. The hearts were subjected to 15 minutes of IR to induce myocardial damage. Cardiac functions including heart rate (HR), resting and developed tension, and rate of change of contraction (+dP/dt max ) were recorded. Cardiac injury biomarkers lactate dehydrogenase (LDH) and creatine kinase (CK-MB) were measured in the heart perfusate. Levels of the antioxidant enzymes reduced glutathione (GSH) and malondialdehyde (MDA) were measured. Hematoxylin and eosin (H&E) staining was also performed. Results:After IR injury, a decrease in HR and +dP/dt max in hearts from diabetic rat was seen compared to healthy rat hearts, which was reversed by phloroglucinol treatment. Myocardial infarct size, measured by H&E staining, was increased in diabetic rats compared to healthy rats and an increase in the activity of LDH and CK-MB in the heart perfusate in diabetic rats was decreased by phloroglucinol treatment.An increase in MDA levels and a decrease in levels of antioxidant enzymes were observed in diabetic rats, which was reversed with phloroglucinol treatment. Conclusion:Phloroglucinol treatment has potential therapeutic promise in the treatment of MRI in diabetes. K E Y W O R D SLangendroff apparatus, myocardial reperfusion injury, phloroglucinol, streptozotocin | 211 PRANAV NAYAK et Al.
Diabetes mellitus (DM) prevalence is increasing at an alarming rate as it was 381 million people globally in 2013 and is estimated to be 463 million people in 2019 rising to 578 million by 2030. It is a disease with high rate of complications such as neuropathy, nephropathy, retinopathy, erectile dysfunction etc. 1,2 Diabetic neuropathy is a family of disorders that damage the different regions of the nervous system, either individually or in combination. It affects pain fibres, motor neurons and autonomic nervous system. 3 It results in large economic costs for its care. [4][5][6] The various kind of neuropathies include peripheral neuropathy, proximal neuropathy, autonomic neuropathy and focal neuropathy. 7 There are a number of reasons for the pathogenesis of diabetic neuropathy and polyol pathway of glucose metabolism is thought as one of the major mechanism. 8 Peripheral neuropathy is a type of nerve damage that usually affects feet and legs and sometimes hands and arms. 9 It is proved that reactive oxygen species (ROS) plays a significant role in the pathophysiology of neuropathic pain in diabetes. 10 Out of all diabetic patients, 50% of patients develop neuropathy and painful neuropathy ranges from 10% to 20% in patients with diabetes. Diabetic patients can experience nerve problems at any time and the problem increases with age, weight and duration. 5 The complications across various countries varies from 10% to 30% and it is higher in developed countries than in developing countries. These complications can lead to painful symptoms and can affect quality of life of the patient. The treatment for the painful diabetic
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