Adjusting vascular permeability, leukocyte infiltration, and microglial cell activation to rescue dopaminergic neurons in rodent models of Parkinson's disease

被引:10
作者
Cai, Hua-Ying [1 ]
Fu, Xiao-Xiao [2 ]
Jiang, Hong [3 ]
Han, Shu [2 ]
机构
[1] Zhejiang Univ, Sir Run Run Shaw Hosp, Med Coll, Dept Neurol, Hangzhou, Peoples R China
[2] Zhejiang Univ, Med Coll, Inst Anat & Cell Biol, Hangzhou, Peoples R China
[3] Zhejiang Univ, Sir Run Run Shaw Hosp, Med Coll, Dept Electrophysiol, Hangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
ALPHA-V-BETA-3 INTEGRIN PEPTIDE; ANGIOPOIETIN-1; MODULATION; MPTP; EXPRESSION; DEMENTIA; DYSTONIA; LRRK2; MICE; C16;
D O I
10.1038/s41531-021-00233-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Animal studies have indicated that increased blood-brain barrier (BBB) permeability and inflammatory cell infiltration are involved during the progression of Parkinson's disease (PD). This study used C16, a peptide that competitively binds to integrin alpha(v)beta(3) and inhibits inflammatory cell infiltration, as well as angiopoietin-1 (Ang-1), an endothelial growth factor crucial for blood vessel protection, to reduce inflammation and improve the central nervous system (CNS) microenvironment in murine models of PD. The combination of C16 and Ang-1 yielded better results compared to the individual drugs alone in terms of reducing dopaminergic neuronal apoptosis, ameliorating cognitive impairment, and electrophysiological dysfunction, attenuating inflammation in the CNS microenvironment, and improving the functional disability in PD mice or rats. These results suggest neuroprotective and anti-inflammatory properties of the C16 peptide plus Ang-1 in PD.
引用
收藏
页数:16
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