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

Acta Cirúrgica Brasileira
Didem OnkSüheyla Ünver

Abstract

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. 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. 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. The melatonin caused an increase in antioxidant capacity and decreased the expression of cleaved-caspase 3.

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Citations

Apr 30, 2020·International Reviews of Immunology·Alex ShneiderAnna Vakhrusheva
Feb 28, 2020·Oxidative Medicine and Cellular Longevity·Mohammed S AleissaMohamed M Abdel-Daim
Mar 8, 2019·Acta Cirúrgica Brasileira·Changxia DongYuanbin Li
Mar 26, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Gianluigi MazzoccoliVictoria Polyakova
Sep 29, 2020·Pathology, Research and Practice·Nazila Fathi MaroufiMohammad Nouri

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis