Gezen-Ak Duygu, Dursun Erdinç, Yilmazer Selma
Department of Medical Biology, İstanbul University Faculty of Medicine, İstanbul, Turkey.
Noro Psikiyatr Ars. 2014 Jun;51(2):157-162. doi: 10.4274/npa.y7076. Epub 2014 Jun 1.
Vitamin D, the main function of which is thought to be the maintenance of calcium and phosphate homeostasis and bone structure, has been shown in recent studies to have important roles in brain development as well. A certain vitamin D receptor (VDR) gene haplotype was reported, for the first time by our group, to increase the risk of developing Alzheimer's disease. Our studies also showed that vitamin D prevents beta amyloid-induced calcium elevation and toxicity that target nerve growth factor (NGF) release in cortical neurons; beta amyloid suppresses VDR expression and the disruption of vitamin D-VDR pathway mimics beta amyloid-induced neurodegeneration. In this study, our aim was to investigate the effects of vitamin D on the NGF release from hippocampal neurons.
Primary hippocampal neuron cultures that were prepared from 18-day-old Sprague-Dawley rat embryos were treated with vitamin D for 48 hours. The alteration in the NGF release was determined with ELISA. Cytotoxicity tests were also performed for all groups.
The NGF release in vitamin D-treated group was significantly higher than in untreated control group. The protective effect of vitamin D against cytotoxicity was also observed.
Our results indicated that vitamin D regulates the release of NGF, a very important molecule for neuronal survival of hippocampal neurons as well as cortical neurons.
维生素D的主要功能被认为是维持钙和磷的稳态以及骨骼结构，但最近的研究表明它在大脑发育中也具有重要作用。我们团队首次报道了某种维生素D受体（VDR）基因单倍型会增加患阿尔茨海默病的风险。我们的研究还表明，维生素D可防止β淀粉样蛋白诱导的钙升高以及针对皮质神经元中神经生长因子（NGF）释放的毒性；β淀粉样蛋白会抑制VDR表达，而维生素D-VDR途径的破坏会模拟β淀粉样蛋白诱导的神经退行性变。在本研究中，我们的目的是研究维生素D对海马神经元释放NGF的影响。
用维生素D处理从18日龄的Sprague-Dawley大鼠胚胎制备的原代海马神经元培养物48小时。用酶联免疫吸附测定法（ELISA）测定NGF释放的变化。还对所有组进行了细胞毒性测试。
维生素D处理组的NGF释放明显高于未处理的对照组。还观察到维生素D对细胞毒性的保护作用。
我们的结果表明，维生素D调节NGF的释放，NGF是海马神经元以及皮质神经元神经元存活的非常重要的分子。
