颈上交感神经节和单涎酸神经节苷脂联合移植抗帕金森病的实验研究

目的：观察颈上交感神经节（SCG）和单涎酸神经节苷酯（GM1）联合植入帕金森病（PD）大鼠脑内的抗PD效果及移植物的存活情况。方法：将用酶消化法制成的同种大鼠SCG细胞悬液和GM1立体定向植入PD大鼠损毁侧尾壳核内，比较单纯细胞移植组，联合移植组，上清液组和非移植组间及移植前，后诱发旋转行为的变化，移植6个月后移植区行组织学检查（HE，TH染色）。结果：两个实验组中的PD大鼠移植后的旋转行为较移植前和对照组明显改善，其中尤以联合移植组的旋转行为减少最为明显，而两个对照组的改善不明显，脑切片组织学观察可见实验组移植区内有存活良好的TH阳性细胞，联合移植组中的阳性细胞数目明显多于单纯细胞移植组。结论：1．GM1可提高SCG细胞在受体脑内的存活率，2．同种成年大鼠SCG细胞植入PD大鼠脑内可以存活，并可纠正PD大鼠的异常旋转行为。

Experimental study of cotransplant of allogeneic superior cervical ganglion and monosialoganglioside into the brain of rat model of Parkinson disease

Objective In order to investigate the effects of cotransplant of superior cervical ganglion (SCG) and monosialoganglioside (GM 1) into the brain of rat model of Parkinson disease (PD) and the survival of the graft.Methods The enzyme digested allogeneic SCG cell suspension and GM 1 were stereotaxically transplanted into the caudate putamen on the lesioned side of the PD rats. The rotational behavior changes among the groups of the solo transplant,co transplant,supernatant transplant and no transplant before and after transplantation were compared.24 weeks after,all of the rats were sacrificed for histological examination using HE and TH immunohistochemical staining.Results In the two cell transplant groups,the rotational behavior of the PD rats were obviously improved as compared with those two groups before transplantation and the two control groups.The improvement of the rotational asymmetry in the co graft group was better than the solo graft group.There were no significant improvement of the rotational behavior in the supernatant group and the no graft group.Immunocytochemical staining showed that a lot of TH positive cells were distributed in the implanted areas of the cell graft groups.The number of positively stained cells in the co graft group was much more than that in the solo graft group.Conclusions 1.GM 1 can increase the survival of SCG cells and enhance their function.2.Transplanted allogeneic SCG cells can survive in host environment and ameliorate behavioral deficits of PD.