自主神经病变是糖尿病最常见的并发症之一。颈上神经节(SCG)和星状神经节(SG)等颈部交感神经节的节后纤维参与心脏功能调节。本项目将2型糖尿病大鼠模型心功能异常变化与SCG及SG中P2X3、P2Y12受体表达研究相结合，了解其与P2受体的相关性。外周神经损伤激活卫星胶质细胞(SGC)导致神经元-SGC间形态与功能异常变化，阻抑此变化可减少神经损伤模型动物初级感觉神经元的异常放电。项目假设P2受体介导糖尿病引发神经元-SGC间异常作用，导致病理性损害。预实验显示糖尿病模型大鼠SCG和SG神经元中P2X3、SGC中P2Y12受体（与SGC标志物GFAP共表达）水平上调。研究用2型糖尿病大鼠模型、高糖高脂细胞损伤模型观察糖尿病引起神经元-SGC间的病理变化是否涉及心功能异常的病理机制，通过阻抑P2X3、P2Y12受体了解对以上病理变化的影响及机理，为探寻糖尿病引起交感神经损伤的防治提供实验基础。

Cervical sympathetic ganglion postganglionic fibers including superior cervical ganglia (SCG) and stellate ganglia (SG) were involved in the regulation of cardiac function. Diabetic cardiac sympathetic neuropathy (DCSN) is a common complication. The project will observe the changes of cardiac dysfunction in type 2 diabetic rat model in combined with the expression changes of P2X3, P2Y12 receptors in SCG and SG to understand the relevance between P2X3, P2Y12 receptors and cardiac dysfunction caused by diabetic injury. Peripheral nervous injury causes abnormal neuron- satellite glial cells (SGC) interactions. Blocking abnormal neuron-SGC interactions reduced sensory neuron abnormal firing in nervous injury models. The project assumption is that P2 receptor-mediated abnormal interactions between neurons-SGC induced by diabetic injury, leading to pathological changes of cervical sympathetic ganglia. Pre-experiments showed the upregulated expression of neuron P2X3 receptor, SGC P2Y12 receptor (P2Y12 co-expressed with SGC marker GFAP) in SCG and SG of type 2 diabetic rat model. In our project, abnormal interactions between neurons and SGCs caused by diabetic injury will be observed by application of diabetic rat model and cell model treated with high sugar and high fat, and whether the pathological changes are involved in the mechanism of cardiac dysfunction. By inhibiting P2X3, P2Y12 receptors, we will observe how to affect these abnormal changes and its mechanism, which will be benefit to explore a new target for prevention and treatment of diabetic cardiac sympathetic neuropathy.