炎症
创伤性脑损伤
神经炎症
氨基酸
内生
化学
小胶质细胞
程序性细胞死亡
医学
生物化学
细胞凋亡
免疫学
精神科
作者
Cong Wei,Peipei Li,Lixin Liu,Hong Zhang,Tianyu Zhao,Yongming Chen
出处
期刊:Biomacromolecules
[American Chemical Society]
日期:2023-01-11
卷期号:24 (2): 909-920
被引量:8
标识
DOI:10.1021/acs.biomac.2c01334
摘要
Following brain trauma, secondary injury from molecular and cellular changes causes progressive cerebral tissue damage. Acute/chronic neuroinflammation following traumatic brain injury (TBI) is a key player in the development of secondary injury. Rapidly elevated cell-free DNAs (cfDNAs) due to cell death could lead to production of inflammatory cytokines that aggravate TBI. Herein, we designed poly(amino acid)-based cationic nanoparticles (cNPs) and applied them intravenously in a TBI mice model with the purpose of scavenging cfDNA in the brain and suppressing the acute inflammation. In turn, these cNPs could effectively eliminate endogenous cfDNA, inhibit excessive activation of inflammation, and promote neural functional recovery.
科研通智能强力驱动
Strongly Powered by AbleSci AI