基于帕金森病脑线粒体功能的刺五加有效组分干预作用及S100B新靶标的构建

已完成刺五加有效组分的脑内药动学（生理和病理状态下）及体内外代谢研究（血液、胆汁、尿液及粪便）；增加并完成了其肠道菌群代谢研究和刺五加有效组分治疗PD的主要药效学及机制研究；正在进行刺五加有效组分对正常和模型机体整体内源性代谢轮廓的干预研究。已发表国家核心期刊文章5篇；SCI文章3篇；获得专利1项。新项目将在原有研究基础上以对PD病区的作用机制为主线，以脑线粒体功能为切入点，从线粒体功能、超微结构改变、抗氧化能力及线粒体蛋白（Parkin、PINK1和DJ-1）表达四大方面探讨刺五加有效组分对PD模型脑线粒体的干预作用，这可能为阐明PD 发病机制及研制有效预防治疗PD 药物提供重要的依据；沿用代谢组学方法，首次进行刺五加有效组分治疗PD的脑代谢组学研究，从脑代谢物组变化角度揭示刺五加有效组分治疗PD的作用机制；并首次引入S100B 蛋白进行中药的干预作用研究，构建PD的S100B新靶标。

In present National Natural Science Foundation of Youth Science Fund, research on brain pharmacokinetics of extract of Acanthopanax senticosus harms(EAS) by UPLC-TOF/MS and microdialysis (in physiologic and pathological state), and research on EAS’s metabolism in vivo and vitro (blood, bile, urine, feces) have been finished. Moreover, research on intestinal flora metabolism, main pharmacodynamics on PD of EAS and its mechanism (DA, HVA, DRD1 ,DRD2 and etc.) have been increased and finished. At present, intervention study of EAS on overall endogenous metabolic profile in normal and model organism are being carried out. There are 5 national core journal articles and 3 SCI articles have been published, and obtain 1 patent. In new project, based on original research, to the mechanism of action on infected zone of PD as the main line and the brain mitochondrial function as the breakthrough point, investigate the intervention study of EAS on brain mitochondria in PD model from four aspects: Mitochondrial function, Ultrastructural changes, oxidation resistance and expression of Mitochondrial proteins(Parkin,PINK1 and DJ-1), and this may be the important basis to clarify the nosogenesis of PD and prepare preventive and therapeutical drug on PD effectively. Based on metabolomics, investigate brain metabolomics of EAS on PD for the first time. From the angle of brain metabolomics, clarify the mechanism of EAS on PD, and introduce S100B to investigate the intervention of traditional Chinese medicine, and build a new target of PD.