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神经营养素 3(neurotrophin 3,NT3)作为螺旋神经节细胞特异的营养因子 ,可有效地支持内耳传入神经元的存活 ,因此有望成为治疗因其退变而引起的感音性神经性耳聋的有效因子。实验采用腺病毒介导lacZ基因 ,检测了外源基因在豚鼠内耳中的长期表达。用噪音制备了豚鼠耳聋模型 ,在噪音损伤后第 7天 ,通过圆窗膜注入 1× 10 8重组腺病毒。注入神经营养素 3重组腺 (Ad NT3)的组为实验组 ,注入Ad lacZ的为对照组。 4周后 ,经NT3抗体免疫细胞化学染色可见 ,在注入Ad NT3病毒的实验组中 ,在内耳多种细胞中有明显的NT3蛋白的表达。HE染色显示 ,注射Ad lacZ组的豚鼠耳蜗螺旋神经节细胞明显退变 ,螺旋神经节内细胞间隙拉大 ,细胞密度明显低于注射Ad NT3实验组动物 (P <0 .0 1)。这一结果说明 ,腺病毒介导的NT3基因可长期表达于内耳中 ,并且可在噪音引起毛细胞死亡后有效地抑制螺旋神经节细胞的退变。
Neurotrophin 3 (NT3), as a specific trophic factor of spiral ganglion cells, can effectively support the survival of afferent neurons in the inner ear and therefore is expected to be effective in treating sensorineural neuropathy due to degeneration factor. The adenovirus-mediated lacZ gene was used to test the long-term expression of foreign genes in the inner ear of guinea pigs. A guinea pig model of deafness was made with noise. On day 7 after noise injury, 1 × 10 8 recombinant adenovirus was injected through the round window membrane. The group injected with Ad Nt3 recombinant adenovirus (Ad NT3) was the experimental group, and the group injected with AdlacZ was the control group. After 4 weeks, the NT3 antibody immunocytochemical staining showed that in the experiment group injected with Ad NT3 virus, there were obvious NT3 protein expression in various inner ear cells. Hematoxylin and eosin staining revealed that the spiral ganglion cells of guinea pigs in Ad lacZ group were significantly degenerated, and the interstitial spaces in the spiral ganglion were enlarged and the cell density was significantly lower than that in Ad NT3 injection group (P <0.01). This result indicates that the adenovirus-mediated NT3 gene can be expressed in the inner ear for a long time and effectively inhibit the degeneration of spiral ganglion cells after the noise-induced hair cell death.