心脏交感神经重构是导致恶性心律失常的重要因素，而心肌组织中NGF水平的升高是导致心肌组织局部神经再生的直接因素。目前对心肌细胞内NGF表达的调控机制认识仍不明确。申请人在前期研究中发现心脏TRPV1受体的激活能够上调缺氧小鼠心肌细胞中NGF的表达，其机制可能是通过调控c-fos基因而实现。本课题拟就这一调控关系的细胞内机制开展进一步研究。计划采用小鼠原代心肌细胞，比较野生型小鼠和TRPV1敲除小鼠在不同干预方法下（对信号通路各环节进行调控）心肌细胞内NGF mRNA 表达情况和蛋白水平。同时采用Western Blotting、RT-PCR、ELISA、CHIP等方法监测下游信号通路各环节蛋白激活情况，以及相关蛋白在转录水平和蛋白水平的变化。随后采用心肌细胞与小鼠交感神经细胞共培养模型，比较不同干预条件下野生型小鼠和TRPV1敲除小鼠组NGF表达差异对交感神经增生的影响。

Cardiac sympathetic nerve remodeling is an important factor of malignant arrhythmia, and the level of NGF in myocardium is a direct factor leading to local nerve regeneration. At present, the understanding of the regulatory mechanism of NGF in cardiac myocytes is still unclear. In the previous studies, the activation of cardiac TRPV1 receptor could upregulate the expression of NGF in cardiomyocytes, which may be regulated by c-fos gene. This study is to carry out further research on the intracellular mechanism of this regulatory relationship. The primary cardiomyocytes of mice were used to compare the expression of NGF mRNA and protein level in cardiac myocytes under different intervention methods (regulating each link of regulatory signaling pathway) in wild type mice and TRPV1 knockout mice. Meanwhile, Western Blotting, RT-PCR, ELISA and CHIP were used to monitor the regulation of protein activation and related gene transcription and protein levels, as well as transcriptional activity. Subsequently, a co-culture model of cardiac myocytes and mouse sympathetic neurons was used to compare the effects of NGF expression on sympathetic nerve proliferation in wild type mice and TRPV1 knockout mice under different intervention.