Department of Anatomy, College of Veterinary Medicine and Research Institute of Life Science, Gyeongsang National University, Jinju 660-701, South Korea.
Neuroscience. 2011 Feb 3;174:171-7. doi: 10.1016/j.neuroscience.2010.11.021. Epub 2010 Nov 24.
Nicotinamide exerts a potent neuroprotective effect against ischemia-induced brain injury. We identified proteins that were differentially expressed by nicotinamide treatment in ischemic brain injury. Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Adult male Sprague-Dawley rats were treated with vehicle or nicotinamide (500 mg/kg) 2 h after the onset of MCAO. Brains were collected 24 h after MCAO and cerebral cortex regions were isolated. Protein spots with different intensities between vehicle- and nicotinamide-treated groups were detected using two-dimensional gel electrophoresis and identified by mass spectrometry. Among these proteins, γ-enolase, protein phosphatase 2A (PP2A) subunit B, and peroxiredoxin-2 (Prx-2) were significantly decreased in the vehicle-treated group compared to the nicotinamide-treated group. These identified proteins mediate cell differentiation and stabilization, and play a role as antioxidant enzymes. In contrast, 60 kDa heat shock protein (Hsp 60) was significantly increased in vehicle-treated animals, while nicotinamide prevented the injury-induced increase of this protein. These results suggest that nicotinamide mediates neuroprotective effects by up- and down-regulation of various specific proteins.
烟酰胺对缺血性脑损伤具有很强的神经保护作用。我们鉴定出了烟酰胺处理在缺血性脑损伤中差异表达的蛋白质。通过大脑中动脉闭塞（MCAO）诱导局灶性脑缺血。MCAO 发作后 2 小时，成年雄性 Sprague-Dawley 大鼠用载体或烟酰胺（500mg/kg）处理。MCAO 后 24 小时收集大脑，并分离大脑皮质区域。使用二维凝胶电泳检测载体和烟酰胺处理组之间强度不同的蛋白质斑点，并通过质谱鉴定。在这些蛋白质中，与烟酰胺处理组相比，载体处理组中的γ-烯醇酶、蛋白磷酸酶 2A（PP2A）亚基 B 和过氧化物酶-2（Prx-2）显著减少。这些已鉴定的蛋白质介导细胞分化和稳定，并作为抗氧化酶发挥作用。相比之下，载体处理动物中的 60kDa 热休克蛋白（Hsp 60）显著增加，而烟酰胺可防止该蛋白因损伤而增加。这些结果表明，烟酰胺通过上调和下调各种特定蛋白质来介导神经保护作用。
