Degradable Poly(amino acid) Vesicles Modulate DNA-Induced Inflammation after Traumatic Brain Injury.
Cong WeiPeipei LiLixin LiuHong ZhangTianyu ZhaoYongming ChenPublished in: Biomacromolecules (2023)
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.
Keyphrases
- traumatic brain injury
- cell free
- oxidative stress
- amino acid
- cell death
- liver failure
- drug induced
- circulating tumor
- severe traumatic brain injury
- cerebral ischemia
- diabetic rats
- respiratory failure
- resting state
- aortic dissection
- multiple sclerosis
- single molecule
- subarachnoid hemorrhage
- cell proliferation
- physical activity
- body mass index
- sensitive detection
- high glucose
- blood brain barrier
- quantum dots
- brain injury
- insulin resistance
- inflammatory response
- extracorporeal membrane oxygenation