Effect of melatonin on antioxidant capacity, inflammation and apoptotic cell death in lung tissue of diabetic rats

Abstract Purpose: To investigate the effects of melatonin on antioxidant capacity, inflammation and apoptotic cell death (through expression of cleaved-caspase 3) in lung tissue samples of diabetic rats. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control group) was made up of healthy rats. Group 2 (diabetes group) received streptozotocin at a dose of 50 mg/kg/day for 5 days.Group 3 (diabetes plus melatonin group) received streptozotocin at a dose of 50 mg/kg/day for 5 days and then they received melatonin at a dose of 20 mg/kg/day between 28thand 35thdays of the study. Results: Tissue MDA and MPO levels were found to be significantly higher in diabetes group compared to control group (p<0.05) whilst administration of melatonin was found to significantly lower this increase down to normal levels (p<0.05). Bronchus associated lymphoid tissue (BALT) was more severe in diabetics whereas administration of melatonin alleviated this hyperplasia. Cleaved caspase 3 activity was severe in hyperplastic BALT in diabetic rats however in lowered down to moderate level when melatonin was administered. Conclusion: The melatonin caused an increase in antioxidant capacity and decreased the expression of cleaved-caspase 3.

Coronary Artery Disease, Hyperlipidemia, Microorganisms and Statins.

Coronary artery disease is a leading cause of death in the world. İnflammation has an important role in the pathogenesis of atherosclerosis. We have known that microorganisms are responsible in atherosclerosis and since they have found in atherosclerotic plaques. Many studies on the effectiveness of statins in atherosclerosis treatment support that besides the antilipidemic activity of the statins, their pleiotropic activities (regulating endothelial function, stabilization of the plaque, decreasing oxidative stress, anti-inflammatory activity, decreasing thrombogenic response to inflammation and immunomodulatory activity) have an important role in their effectiveness on mortality and morbidity. As a result, it has been understood that microorganisms have an important role in the etiology of coronary artery occlusion. It has been found that hyperlipidemia is an early defense system against microbial damage of the vessel wall. Suppression of hyperlipidemia-related atherosclerosis or atherosclerotic plaque by drugs or methods not having antimicrobial activity is thought to trigger sudden vessel occlusion. Causes of sudden death associated with coronary artery and other forms of atherosclerosis have still not been fully elucidated. This study proposes that hyperlipidemia and atherosclerosis develop as a defense reaction to damage caused by micro-organisms in the coronary arteries. It also proposes that the treatment of atherosclerosis-associated subtotal obstruction of the coronary artery with hypolipidemic drugs exhibiting no antimicrobial activity, or in other ways (extreme weight loss in a short period of time), may cause sudden death.