帕金森氏病是常见的中枢神经系统变性疾病，以黑质和纹状体多巴胺能神经元慢性进行性缺失为主要病理特点，伴随神经系统免疫炎症反应。除胶质细胞内源性激活外，血脑屏障功能失调所介导的外周免疫细胞血管外渗及中枢浸润也是神经炎症反应的主要环节。申请者前期申请的靶向血管通透性的复合专利药物（血管生成素Ang-1和C16多肽）在多发性硬化及视神经脊髓炎等模型中均被证明可以通过调节血管通透性和抑制胶质细胞活化来改善中枢神经系统炎性微环境。本研究将在前期研究基础上，进一步探讨复合专利药物对帕金森氏病的症状改善及炎症微环境的影响，解析其调节血管通透性和抑制胶质细胞活化的相关信号通路，阐明其作用机制，并检测其可能产生的毒副作用，通过改良剂型以提高应用效率，为将来的成果转化，向临床前实验过渡打下坚实的基础。

Parkinson's disease is a common degenerative disease of the central nervous system. Chronic progressive loss of dopaminergic neurons in substantia nigra and striatum, and the accompanied immune inflammation in the nervous system are the main pathological features. In addition to endogenous activation of glial cells, vascular extravasation and central infiltration of peripheral immune cells mediated by dysfunction of blood-brain barrier are also the main steps of neuroinflammatory response. Previous patented drugs targeting vascular permeability (Ang-1 and C16 polypeptide) have been shown to alleviate the inflammatory microenvironment of the central nervous system by regulating vascular permeability and inhibiting glial cell activation in multiple sclerosis and optic neuromyelitis models. On the basis of the serious investigations, this study will further explore the effects of patented drugs on the improvement of symptoms and inflammatory microenvironment of Parkinson's disease, elucidate the related signaling pathways of vascular permeability and glial cell activation, and further clarify its possible toxic and side-effects to improve its efficacy through ameliorating the form of drug. All of these will lay a strong foundation for clinic research and application in the future.