糖痹康调节AMPK/PGC-1α/SirT3信号通路干预线粒体应激防治糖尿病周围神经病变的机制研究

糖尿病周围神经病变（DPN）发病率和致残率高，中医药对改善DPN临床症状疗效显著，科学内涵亟待阐明。前期研究临床有效中药方糖痹康（专利号：ZL200810167551.1）可通过减少氧化应激引起的雪旺细胞凋亡实现DPN神经保护作用。最新研究表明，线粒体应激在DPN发生发展过程中处于核心地位，调节AMPK/PGC-1α/SirT3信号通路改善线粒体应激损伤是治疗DPN的关键分子机制，那么“糖痹康抗氧化应激诱导雪旺细胞凋亡的作用是否与调节AMPK/PGC-1α/SirT3信号通路减轻线粒体应激的分子机制相关”？预实验发现糖痹康可通过调节脂肪酸降解及代谢对DPN大鼠起到神经保护作用。由此我们以“雪旺细胞线粒体应激”为切入点，利用脂质组学等技术和线粒体缺陷动物模型，拟从整体和细胞水平探讨糖痹康对DPN神经保护作用机理，以期为糖痹康治疗DPN提供理论和实验依据，为中药抗DPN研究提供新思路。

Diabetic peripheral neuropathy (DPN) has a high morbidity and disability rate. Traditional Chinese Medicine (TCM) has a significant effect for on TangBiKang (PATENT NO: ZL200810167551.1), which is valid in clinical medicine, could protect nerve of DPN by decreasing Schwann cells apoptosis which is due to oxidative stress. The updated pathology research has indicated that mitochondrial stress is at the core in the course of the occurrence and development of DPN. Regulating the AMPK/PGC-1α/Sirt3 signaling pathway to remitting mitochondrial stress injury is the key molecular mechanism of the treatment for DPN. Then “TangBiKang could anti-oxidative stress to induce the apoptosis of Schwann cells, is that related to the mechanism that TangBiKang can regulate the AMPK/PGC-1α/Sirt3 signaling pathway to release mitochondrial stress?” The pre-experimental had found that TangBiKang may protect the rats’ nerve which had get DPN by regulating fatty acid degradation and metabolism. As a result, we regard mitochondrial stress of Schwann cell as a starting point to discuss the mechanism of the effect of protection for DPN in vivo and cell level by lipidomics technology and mitochondrial defect in animal model. So that we can provide a basis for theoretical and experimental evidence of the TangBiKang, offer new ideas for the study on curing DPN by TCM.