Cammer Wendy
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Brain Res Bull. 2002 Sep 30;58(6):587-92. doi: 10.1016/s0361-9230(02)00830-4.
Tumor necrosis factor-alpha (TNF-alpha) retards the rate of terminal maturation of oligodendrocytes in vitro. The following respective compounds were used along with TNF-alpha in order to try and restore the normal rate of maturation: (1). the antioxidant, coenzyme Q(10) (CoQ(10)); (2). the antioxidant, N-acetyl cysteine (NAC); (3). creatine, which helps to preserve cellular energy; and (4) S-adenosyl methionine (SAM), which contributes to the biosynthesis of lipids and proteins. Of these compounds, only CoQ(10) or NAC was able to restore the numbers of mature myelin basic protein-positive cells and the ability of the oligodendrocytes to form membrane sheets. If TNF-alpha treatment causes oxidative damage by compromising oxidative metabolism in oligodendrocytes, increasing products of lipid peroxidation and/or generating radical oxygen species that can interfere with maturation signals, CoQ(10) and NAC may protect oligodendrocytes by reversing one or more of those destructive processes during terminal maturation.
肿瘤坏死因子-α（TNF-α）在体外会延缓少突胶质细胞的终末成熟速率。为尝试恢复正常的成熟速率，将以下各化合物与TNF-α一起使用：（1）抗氧化剂辅酶Q10（CoQ10）；（2）抗氧化剂N-乙酰半胱氨酸（NAC）；（3）有助于维持细胞能量的肌酸；以及（4）对脂质和蛋白质生物合成有贡献的S-腺苷甲硫氨酸（SAM）。在这些化合物中，只有CoQ10或NAC能够恢复成熟髓鞘碱性蛋白阳性细胞的数量以及少突胶质细胞形成膜片的能力。如果TNF-α处理通过损害少突胶质细胞的氧化代谢、增加脂质过氧化产物和/或产生可干扰成熟信号的活性氧来造成氧化损伤，那么CoQ10和NAC可能通过在终末成熟过程中逆转这些破坏过程中的一个或多个来保护少突胶质细胞。
