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
- drug induced
- cell death
- liver failure
- circulating tumor
- severe traumatic brain injury
- diabetic rats
- respiratory failure
- white matter
- cerebral ischemia
- resting state
- multiple sclerosis
- subarachnoid hemorrhage
- aortic dissection
- single molecule
- signaling pathway
- functional connectivity
- mild traumatic brain injury
- living cells
- type diabetes
- metabolic syndrome
- hepatitis b virus
- intensive care unit
- lipopolysaccharide induced
- weight gain
- extracorporeal membrane oxygenation
- sensitive detection
- cognitive impairment
- fluorescent probe
- adipose tissue
- inflammatory response
- physical activity
- skeletal muscle
- mechanical ventilation