免疫机制与帕金森病关系的研究

A study of relationship between immune mechanism and Parkinson's disease

目的 探讨免疫机制与帕金森病 (PD)发病的相关性。方法 采用PD患者的血清IgG建立PD的细胞模型 ,将纯化的PD患者、疾病对照组患者及正常人的血清IgG或 /及补体加入大鼠胚胎中脑神经元 胶质细胞混合培养体系中 ,通过MTT法检测细胞活力 ,免疫细胞化学法评价多巴胺 (DA)能细胞的数目、形态。结果 单独PDIgG(6 0 μg/ml)或补体对原代中脑神经元 胶质细胞混合培养体系中的DA能神经元的数目、形态无明显影响 (P >0 0 5 ) ;当培养体系同时接受二者处理时 ,抗酪氨酸羟化酶 (TH)阳性细胞数明显减少 (P <0 0 1) ,突起明显减少和缩短 ,β tubulin阳性细胞数和形态无明显变化 (P >0 0 5 ) ,总的细胞活力无明显下降(P >0 0 5 ) ,PDIgG(0、2 0、6 0、10 0 μg/ml)依赖补体对DA能神经元的毒性作用呈剂量依赖性。疾病对照组和正常对照组的血清IgG即使在补体存在时对TH阳性细胞数、形态也无明显影响 (P >0 0 5 )。结论 在补体存在时 ,用PDIgG可建立PD的细胞模型 。

Objective To explore the relationship between immune mechanism and the pathogenesis of Parkinson's disease(PD).Methods IgGs were purified from serum samples of patients with idiopathic PD, other neurological diseases(DC), and healthy people(NC) using ferric ammonium sulfate precipitation, ion exchange chromatography and filtration dialysis. Rat mesencephalic cells were exposed to IgGs in the presence or absence of complement. The number and morphology of cells were determined by tyrosine hydroxylase(TH) and β-tubulin immunocytochemistry. Cell viability was measured by MTT assay.Results The number and morphology of rat embryo mesencephalic dopaminergic neurons were not altered following exposure to PD IgG(60 μg/ml) or complement respectively( P>0.05). After the exposure to PD IgG together with complement, the number of TH(+) neurons was significantly decreased( P<0.01). Morphologically, the neurites of TH(+) neurons became fewer and shorter. In contrast, the number of β-tubulin(+) neurons, and cell viability did not change obviously( P>0.05). PD IgG-induced toxicity to dopaminergic neurons was dose-dependent. No alternations in the number, morphology of dopaminergic neurons were found following the exposure of primary mesencephalic neuron-glia cultures to the IgGs from DC and NC, even in the presence of complement( P>0.05). Conclusion An in vitro model of PD can be produced by serum IgG with PD patients in the presence of complement. The immune mechanism may be involved in the pathogenesis of PD.