Uncontrolled diabetes mellitus (DM) is linked to attentional deficits and cognition deterioration. The neurohormone melatonin is an endogenous synchronizer of circadian rhythms with multiple protective properties. This research was designed to assess its effect against learning and memory decline in streptozotocin (STZ)-induced diabetic rats. Rats were assigned to control, melatonin-treated control, diabetic, and melatonin-treated diabetic groups. Melatonin was administered i.p. at a dose of 10 mg/kg/day for 47 days. Treatment of diabetic rats with melatonin reversed decline of spatial recognition memory in Y maze, performance of rats in novel object discrimination, and retention and recall in passive avoidance tasks. Furthermore, melatonin appropriately attenuated hippocampal malondialdehyde (MDA) and reactive oxygen species (ROS) and improved superoxide dismutase (SOD) activity and improved mitochondrial membrane potential (MMP) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) with no significant effect on nitrite, glutathione (GSH) and catalase activity. Besides, hippocampal level of acetylcholinesterase (AChE), glial fibrillary acidic protein (GFAP), nuclear factor-kappaB (NF-κB), interleukin 6 (IL-6) and tumor necrosis factor α (TNFα) decreased following melatonin treatment. There was also a reduction of dendritic spines of pyramidal neurons of hippocampal CA1 area in diabetic group that was significantly alleviated upon melatonin treatment. Melatonin could ameliorate learning and memory disturbances in diabetic rats through mitigation of cholinesterase activity, astrocytes, oxidative stress and inflammation and also via upregulation of some antioxidants in addition to its prevention of dendritic spine loss.

中文翻译：

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褪黑激素通过减轻氧化应激和炎症逆转大鼠链脲佐菌素诱导的 1 型糖尿病的认知缺陷

不受控制的糖尿病 (DM) 与注意力缺陷和认知能力下降有关。神经激素褪黑激素是昼夜节律的内源性同步器，具有多种保护特性。本研究旨在评估其对链脲佐菌素 (STZ) 诱导的糖尿病大鼠学习和记忆力下降的影响。大鼠被分配到对照组、褪黑激素治疗对照组、糖尿病组和褪黑激素治疗糖尿病组。褪黑激素以 10 mg/kg/天的剂量 ip 给药，持续 47 天。用褪黑激素治疗糖尿病大鼠逆转了 Y 迷宫中空间识别记忆的下降、大鼠在新物体辨别方面的表现以及被动回避任务中的保留和回忆。此外，褪黑激素适当减弱海马丙二醛 (MDA) 和活性氧 (ROS) 并改善超氧化物歧化酶 (SOD) 活性和改善线粒体膜电位 (MMP) 和核因子（红细胞衍生的 2）样 2（Nrf2），但没有显着影响对亚硝酸盐、谷胱甘肽 (GSH) 和过氧化氢酶活性的影响。此外，褪黑激素治疗后海马的乙酰胆碱酯酶（AChE）、胶质纤维酸性蛋白（GFAP）、核因子-κB（NF-κB）、白介素6（IL-6）和肿瘤坏死因子α（TNFα）水平下降。糖尿病组海马CA1区锥体神经元树突棘也减少，褪黑激素治疗后显着减轻。褪黑激素可以通过减轻胆碱酯酶活性来改善糖尿病大鼠的学习和记忆障碍，