肥胖、高脂血症及其引发的心脑血管疾病已经成为危害中老年人健康的主要疾病。肥胖时血游离脂肪酸上升，炎性细胞因子增加，激活炎症信号通路，诱使机体处于慢性炎症状态。肥胖能够增加交感神经系统兴奋性。颈部交感神经节（颈上神经节和星状神经节）节后神经纤维可影响心脏的交感兴奋传出活动。颈上和星状神经节卫星胶质细胞主要表达P2X4受体，P2X4受体的异常表达与炎症相关。欧前胡素具有抗炎作用。预实验显示欧前胡素抑制肥胖大鼠星状神经节卫星胶质细胞P2X4受体的上调表达，提示欧前胡素可能影响颈部交感神经节P2X4受体介导的肥胖及低度慢性炎症引发心交感神经病理性损伤。本项目通过整体、细胞及分子实验相结合的实验方法研究颈部交感神经节卫星胶质细胞P2X4受体在肥胖及代谢综合征引起的心交感神经病理变化中的作用，观察欧前胡素对P2X4受体介导高脂引起心交感神经病理变化的影响及可能机理。

Cardiovascular and cerebrovascular diseases caused by obesity and hyperlipidemia have become the main diseases endangering the health of middle-aged and elderly people. When obesity occurs, the levels of blood free fatty acids are elevated, inflammatory cytokines are increased, and inflammatory signaling pathways are activated, which lead the body to be in a state of chronic inflammation. Obesity increases the excitability of the sympathetic nervous system. Postganglionic nerve fibers of the cervical sympathetic ganglia (superior cervical ganglion and stellate ganglion) can affect the sympathetic efferent activity of the heart. P2X4 receptors are mainly expressed in satellite glial cells of superior cervical and stellate ganglia, and abnormal expression of P2X4 receptors are related to inflammation. Imperatorin has anti-inflammatory activity. Preliminary experiments showed that imperatorin inhibited the up-regulation of P2X4 receptor expression in the satellite glial cells of stellate ganglia in obese rats, suggesting that imperatorin may influence the cervical sympathetic ganglion P2X4 receptor-mediated obesity and low-grade chronic inflammation-induced cardiac sympathetic neuropathic injury. Applying the experimental approaches at the animal, cellular and molecular levels, this project is aimed to investigate the role of P2X4 receptor of the satellite glial cells of cervical sympathetic ganglia in developing cardiac sympathetic neuropathy induced by obesity and metabolic syndrome, and to explore the effect of imperatorin on the P2X4 receptor-mediated pathological changes of cardiac sympathetic neuropathy induced by hyperlipidemia and its possible underlying mechanism.