Project description:Post-traumatic neuroinflammation is a key driver of secondary injury after traumatic brain injury (TBI). Pyroptosis, a proinflammatory form of programmed cell death, considerably activates strong neuroinflammation and amplifies the inflammatory response by releasing inflammatory contents. Therefore, treatments targeting pyroptosis may beneficially effects for the treatment of secondary brain damage after TBI. Herein, a cysteine-alanine-glutamine-lysine (CAQK) peptide-modified β-lactoglobulin (β-LG) nanoparticle was constructed to deliver disulfiram (DSF), C-β-LG/DSF, to inhibit pyroptosis and decrease neuroinflammation, thereby preventing TBI-induced secondary injury. In the post-TBI mice model, C-β-LG/DSF selectively targets the injured brain, increases DSF accumulation, and extends the time of the systemic circulation of DSF. C-β-LG/DSF can alleviate brain edema and inflammatory response, inhibit secondary brain injury, promote learning, and improve memory recovery in mice after trauma. Therefore, this study likely provided a new approach for reducing the secondary spread of TBI.

2024-01-17 | GSE244966 | GEO

Blood-brain barrier breakdown following traumatic brain injury: a possible role in posttraumatic epilepsy.

Project description: Not available

| S-EPMC3056210 | biostudies-literature

Project description: Not available

| S-EPMC3996118 | biostudies-literature

Post-traumatic peripheral vestibular disorders (excluding positional vertigo) in workers following head injury.

Project description: Not available

| S-EPMC8648866 | biostudies-literature