兔脊髓空洞前状态神经细胞凋亡与Bcl-2、Bax蛋白表达的关系

Neuronal apoptosis and its relationship with Bcl-2 and Bax expressions in experimental presyrinx state of rabbits

目的探讨实验性脊髓空洞前状态（presyinx state）神经细胞凋亡及其与Bcl-2，Bax蛋白表达的关系。方法制作动物模型，用TUNEL法和免疫组化技术检测上颈髓神经细胞凋亡趋势和Bcl-2，Bax表达变化。结果Kaolin（高龄土、白陶土）组动物神经细胞凋亡于术后第1天出现增加。7—14d达高峰。以后逐渐降低，21d仍可见到凋亡发生；Bcl-2和Bax表达则于术后第1天开始增加。第7天达高峰。持续至第14天后下降。但主要以Bax表达增高为著。结论实验性脊髓空洞前状态演变过程中。主要上调其靶基因Bax诱导神经细胞凋亡。参与了脊髓的神经功能损害。

Objective To investigate neuronal apoptosis of presyrinx state and its relationship with Bcl-2 and Bax expression in experimental presyrinx state of rabbits. Methods The experimental syringomyelia models of rabbits were estsblished to detect neuronal apoptosis trend and the changes in expression of Bcl-2 and Bax in cervical cord with TUNEL and immunohistochemistry. Results Neuronal apoptosis in Kaolin group increased from the 1st day, reached its peak during the 7th - 14th day, then began to drop, and until in the 21st day neuronal apoptosis could be observed. Bcl-2 and Bax expressions showed the same tendency, but the increase in expression of Bax was more significant. Conclusions Experimental presyrinx state mainly upregulates its target gene Bax, inducing neuronal apeptosis to involve in nervous function injury.