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早产儿脑损伤问题是围产期医学的热点问题。早产儿脑损伤多表现为脑白质的损伤,白质损伤也可累及皮质。早产儿脑白质损伤与少突胶质细胞的缺氧缺血易损性有关。研究发现3种中枢神经髓鞘来源的主要髓磷脂相关轴突生长抑制物:髓磷脂相关抑制物(Nogo-A,myelin-associated inhibitors Nogo)、髓鞘相关糖蛋白(myelin-associated glycoprotein,MAG)、少突胶质细胞髓鞘糖蛋白(oligodendrocyte-myelin glycoprotein,OMgp)。Nogo-A、MAG和OMgp可能通过与神经元上的一个共同受体Nogo-66受体(NgR)结合并传导信号级联反应,抑制神经元轴突的生长。通过RNA干扰下调NgR的表达,理论上可以同时减轻这3个髓磷脂相关抑制因子的作用,在缺氧缺血脑损伤后减少神经元的凋亡,促进神经轴突再生,具有很好的应用前景。
Brain injury in preterm infants is a hot issue in perinatal medicine. Brain damage in preterm infants more manifestations of white matter damage, white matter damage can also affect the cortex. Premature children with white matter damage and oligodendrocyte hypoxia-ischemia vulnerability. The study found that three kinds of myelin-derived major myelin-associated axon growth inhibitors: myelin-associated inhibitors Nogo, myelin-associated glycoprotein (MAG) , Oligodendrocyte-myelin glycoprotein (OMgp). Nogo-A, MAG and OMgp may inhibit neuronal axon growth by binding to a common receptor Nogo-66 receptor (NgR) on neurons and transducing a signal cascade. Down-regulation of NgR expression by RNA interference can theoretically alleviate the effects of these three myelin-related inhibitors and reduce neuronal apoptosis and promote axon regeneration after hypoxic-ischemic brain damage, which has a good application prospect.