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目的探讨抑制配对免疫球蛋白B(PirB)的活性能否阻止由髓鞘抑制因子产生的神经再生抑制。方法采用动物体外实验,用出生2日龄SD新生大鼠脑组织行神经元细胞原代培养,进行缺氧缺血处理后,通过免疫组化及RT-PCR方法检查缺氧缺血损伤后神经元细胞内PirB含量的变化,观察加入抗PirB抗体后损伤神经元生长的恢复。结果与对照组相比,PirB mRNA和蛋白在大鼠缺氧缺血损伤组神经元细胞中表达均升高[(3.2±0.5)比(1.0±0.1),(2.5±0.3)比(1.2±0.1),P均<0.05],加入PirB抗体后可促进缺氧缺血损伤神经元生长,轴突再生长度比未加入PirB抗体的缺氧缺血组增加[(298±43)μm比(198±48)μm,P<0.05]。结论抑制PirB可能是促进缺氧缺血损伤神经再生新的治疗方法。
Objective To investigate whether inhibiting the activity of paired immunoglobulin B (PirB) can prevent the inhibition of nerve regeneration by myelin inhibitory factors. Methods In vitro experiments in vivo were performed in neonatal SD rats of 2 days old for primary culture of neuronal cells. After hypoxic-ischemic injury, the neurons were examined by immunohistochemistry and RT-PCR Cell PirB content changes observed after the addition of anti-PirB antibody damage the recovery of neuronal growth. Results Compared with the control group, the expression of PirB mRNA and protein in the neurons of hypoxic ischemic injury group was significantly higher than that of the control group [(3.2 ± 0.5) vs (1.0 ± 0.1), (2.5 ± 0.3) vs (1.2 ± P <0.05). PirB antibody could promote the neuron growth in hypoxic-ischemic injury, the length of axon regeneration increased compared with hypoxia-ischemia group without PirB antibody [(298 ± 43) μm (198 ± 48) μm, P <0.05]. Conclusion Inhibition of PirB may be a new therapeutic method to promote nerve regeneration after hypoxic-ischemic injury.