Jia D, Heng L-J, Yang R-H, Gao G-D
Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an 710038, PR China.
Department of Nutrition and Food Hygiene, The Ministry of Education Key Laboratory of Hazard Assessment and Control in Special Operational Environment, School of Public Health, The Fourth Military Medical University, Xi'an 710032, PR China.
Neuroscience. 2014 Jan 31;258:228-37. doi: 10.1016/j.neuroscience.2013.11.016. Epub 2013 Nov 16.
Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the lipid peroxidation, inflammation and neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. STZ-induced diabetes impaired spatial learning and memory of rats, which was associated with the inflammation, oxidative stress and apoptosis of hippocampal neurons. Fish oil administration ameliorated cognitive deficit, reduced oxidative stress and tumor necrosis factor α (TNF-α), protected the hippocampal neurons by increasing Protein Kinase B (AKT) phosphorylation and decreasing caspase-9 expression. These results suggested that the principle mechanisms involved in the antidiabetic and neuroprotective effect of fish oil were its antioxidant, anti-inflammatory and anti-apoptosis potential, supporting a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications.
先前的研究表明，糖尿病会导致学习和记忆缺陷。然而，糖尿病引起记忆损害的机制尚不清楚。膳食脂肪酸，尤其是多不饱和脂肪酸，已被证明在各种实验条件下可增强学习和记忆并预防记忆缺陷。本研究调查了补充鱼油对链脲佐菌素（STZ）诱导的糖尿病大鼠海马体脂质过氧化、炎症和神经元凋亡的影响。还使用莫里斯水迷宫评估了糖尿病和鱼油治疗对空间学习和记忆的影响。STZ诱导的糖尿病损害了大鼠的空间学习和记忆，这与海马神经元的炎症、氧化应激和凋亡有关。给予鱼油可改善认知缺陷，降低氧化应激和肿瘤坏死因子α（TNF-α），通过增加蛋白激酶B（AKT）磷酸化和降低半胱天冬酶-9表达来保护海马神经元。这些结果表明，鱼油的抗糖尿病和神经保护作用的主要机制是其抗氧化、抗炎和抗凋亡潜力，支持鱼油作为预防和治疗糖尿病并发症辅助疗法的潜在作用。
