Abstract

Hyperglycaemic condition induced oxidative stress in diabetic individuals caused oxidative damages of internal organs, including immune organ spleen. We studied the effects of low doses of melatonin (25, 50, and 100 µg/100g. B.wt./day) on histoarchitecture, oxidative stress, and splenocyte proliferation in streptozotocin-induced diabetic mice. Melatonin significantly resisted the increase in blood glucose levels and showed a dose-dependent effect on circulatory melatonin, body weight, and relative spleen weight in diabetic mice. Exogenous melatonin suppressed the diabetes-induced lipid peroxidation and increased the activity of the antioxidant enzymes and antioxidant GSH in the spleen tissue of diabetic mice in a dose-dependent manner. Melatonin improved the reactivity of Nrf-2 and HO-1 in the spleen of diabetic mice. Melatonin treatment normalised the splenic cellularity and increased the splenocyte proliferation in a dose-dependent manner. The present study may suggest the dose-dependent effect of melatonin in attenuation of oxidative stress and suppression of splenocyte proliferation in diabetic mice.

摘要

高血糖状态在糖尿病个体中诱导的氧化应激引起内脏器官的氧化损伤，包括免疫器官脾脏。我们研究了低剂量褪黑激素（25、50 和 100 µg/100g. B.wt./天）对链脲佐菌素诱导的糖尿病小鼠的组织结构、氧化应激和脾细胞增殖的影响。褪黑激素显着​​抵抗血糖水平的升高，并对糖尿病小鼠的循环褪黑激素、体重和相对脾重表现出剂量依赖性影响。外源性褪黑激素以剂量依赖性方式抑制糖尿病诱导的脂质过氧化并增加糖尿病小鼠脾组织中抗氧化酶和抗氧化谷胱甘肽的活性。褪黑激素改善了糖尿病小鼠脾脏中 Nrf-2 和 HO-1 的反应性。褪黑激素治疗使脾细胞结构正常化并以剂量依赖性方式增加脾细胞增殖。本研究可能表明褪黑激素在减轻糖尿病小鼠的氧化应激和抑制脾细胞增殖方面具有剂量依赖性作用。