二聚糖（Biglycan）不仅是细胞基质中的结构蛋白，还可以作为信号分子发挥作用，与神经突触的稳定性和神经变性疾病的发生发展密切相关。我们前期研究工作显示，在NO诱导神经细胞损伤中，NF-κB活化发挥神经保护效应。基因芯片的结果显示Biglycan是NF-κB的关键下游靶点，因此推测，Biglycan可能通过调控生长和凋亡信号通路而发挥抗NO神经毒性的功能。为此，本课题将选用神经细胞系SHEP-1和原代神经元建立NO损伤模型，利用载体构建，基因转染，流式细胞术，Western Blot, 免疫荧光等细胞生物学和分子生物学技术，综合分析Biglycan在NO诱导神经细胞损伤中的作用以及涉及的关键信号机制，为寻求新靶点治疗神经方面疾病提供理论依据和应用价值。

Biglycan is not only the structural protein of the extracellular matrix, but also can play a important role as a signaling molecule, closely related to the stability of synapses and the development of neurodegenerative diseases. Our previous studies showed that NF-κB activation exerts neuroprotective effects in NO-induced neuronal injury. The further results of microarray analysis showed Biglycan is a key downstream target of NF-κB, so we speculate that Biglycan may protect neuronal cells against NO-induced injury by regulating the growth and apoptotic signaling pathway. To this end, the subject will choose SHEP-1 cells and primary neurons to establish NO damage model. using cell biology and molecular biology techniques including vector construction, gene transfection, flow cytometry, Western Blot, immunofluorescence, we will comprehensively study the function and involved key mechanism of Biglycan in NO-induced neuronal cell death. Our study will provide theoretical basis and practical value for seeking new target in the treatment of neurological diseases.