高血糖会通过氧化应激形成代谢记忆效应，阻断代谢记忆是防治糖尿病周围神经病变(DPN)的关键。氧化应激在DPN发生发展过程中处于核心地位，也是凋亡与自噬重要的诱因。自噬和凋亡在溶酶体-线粒体轴调节下存在交互对话，共同调控细胞功能。本课题组在既往研究基础上从“伏邪理论”着手，认为代谢记忆类似于伏邪在体内伏匿的过程，脏腑功能失调是产生伏邪的基本条件，痰浊、瘀血是伏邪的主要构成部分。本研究通过分子生物学和细胞生物学方法，建立高糖代谢记忆动物和细胞模型，以氧化应激为切入点，从整体、细胞、分子水平研究溶酶体-线粒体轴调节的自噬与凋亡交互对话在代谢记忆所致DPN中的作用，并进一步探讨了基于痰瘀伏邪论治中药糖周通的干预作用及其机制。课题的实施可为糖周通治疗DPN提供理论及实验依据，并为DPN防治提供新的思路和手段，为研发治疗DPN的创新中药奠定基础。

Long term hyperglycemia could lead to metabolic memory via oxidative stress and shut off metabolic memory as early as possible is important to prevent the diabetic peripheral neuropathy (DPN).However, oxidative stress induced by mitocondrial disfunction plays a key role in the in the initiation and progression of DPN,which is an important inducer of apoptosis and autophagy.The balance between apoptosis and autophagy may be regulated by the lysosomal-mitochondrial axis through a cross-talk to prolong cell survival and to limit cell death.Based on our previous study,we put forward that the incubative pathogen prostrate in vivo is similar to the metabolic memory．The pacing factor is viscera disbalance，the principal intergrant are phlegm and haemostasis．In our study,we used animal model of DPN and nervous cells cultured in high glucose to minimic a diabetic condition.The immunohistochemical method, flow cytometry analysis, confocal laser scanning microscope, Western blot and Real-Time Reverse Transcription Polymerase Chain Reaction method were used to investigate the damaging effect of metabolic memory through a cross-talk between autophagy and apoptosis for the peripheral nerve function. More importantly,the protective effect of decoction Tangzhoutong and its molecular mechanisms are also investigated.Our results are both provide a new window and method,but also provide a remarkable evidence in molecular connotation for the therapy of DPN with Tarditional Chinese medicine.