LAUSR

Survival after severe traumatic brain injury (TBI) depends on minimizing or avoiding secondary insults to the brain. Overproduction of reactive oxygen species (ROS) and Ca2+ influx at the damaged site are the key factors that cause secondary injury upon TBI. Herein, a TBI‐targeted lipid covered radical scavenger nanoparticle is developed to deliver nimodipine (Np) (CL‐PPS/Np), in order to inhibit Ca2+ influx in neurons by Np and to scavenge ROS in the brain trauma microenvironment by poly(propylene sulfide)60 (PPS60) and thus prevent TBI‐associated secondary injury. In post‐TBI models, CL‐PPS/Np effectively accumulates into the wound cavity and prolongs the time of systemic circulation of Np. CL‐PPS/Np can markedly protect the integrity of blood‐brain barrier, prevent brain edema, reduce cell death and inflammatory responses, and promote functional recovery after TBI. These findings may provide a new therapy for TBI to prevent the spread of the secondary injury.