中文摘要：

亨廷顿的疾病(HD ) 被 polyglutamine 道的扩大在 huntingtin (htt ) 的 N 终点引起。htt 的变化导致机能障碍和 striatal 和外皮的神经原的早熟的死亡。然而，神经胶质上的 htt 变化的效果仍然保持大部分未知。这研究试图用 adenoviral 向量建立一个神经胶质 HD 模型在老鼠表示野类型、变异的 N 终端 huntingtin 碎片 1552 氨基酸(htt552 ) 主要外皮的星形细胞。我们在星形细胞与 htt552 的表示的 adenoviral 向量，和动力学为星形细胞的感染评估了最佳的条件。星形细胞的多数在感染以后表示了 transgene。在 24 h 感染以后，感染的最高的率是 89 漠 ? 慦桳潩？

英文摘要：

Huntington＇s disease （HD） is caused by an expansion of polyglutamine tract in N-terminus of huntingtin （htt）. The mutation of htt leads to dysfunction and premature death of striatal and cortical neurons. However, the effects of htt mutation on glia remain largely unknown. This study aimed to establish a glia HD model using an adenoviral vector to express wild-type and mutant N-terminal huntingtin fragment 1-552 amino acids （htt552） in rat primary cortical astrocytes. We have evaluated optimal conditions for the infection of astrocytes with adenoviral vectors, and the kinetics of the expression of htt552 in astrocytes. The majority of astrocytes expressed the transgene after infection. At 24 h postinfection, the highest rate of infection was 89 ± 3% for the wild-type （htt552-18Q） with a multiplicity of infection （m.o.i.） of 80, and the highest rate of infection was 91 ± 4% for the mutant type （htt552-100Q） with the same viral dose. The duration of expression of htt552 lasted for about 7 days with a relatively high level from 1 to 4 days post-infection. Mutant huntingtin （htt552-100Q） produced the characteristic HD pathology after 3 days by the appearance of cytoplasmic aggregates and intranuclear inclusions. The result of MTT （3-（4,5- Dimethylthiazol-2-yl）-2,5-diphenyltetrazoliumbromide） assay showed that the inhibition of viability by virus on astrocytes was also dose-dependent. To obtain high infection rate and low toxicity, the viral dose with an m.o.i, of 40 was optimal to our cell model. The present study demonstrates that adenoviral-mediated expression of mutant htt provides an advantageous system for histological and biochemical analysis of HD pathogenesis in primary cortical astrocyte cultures.