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
- resting state
- respiratory failure
- white matter
- cerebral ischemia
- multiple sclerosis
- functional connectivity
- hepatitis b virus
- type diabetes
- signaling pathway
- subarachnoid hemorrhage
- body mass index
- mild traumatic brain injury
- intensive care unit
- weight gain
- skeletal muscle
- adipose tissue
- cognitive impairment
- sensitive detection
- metabolic syndrome
- brain injury
- cell cycle arrest
- mechanical ventilation
- cell proliferation
- pi k akt
- blood brain barrier
- lipopolysaccharide induced
- acute respiratory distress syndrome