2. Academic Validation
  3. A Novel Targeted Nanoparticle for Traumatic Brain Injury Treatment: Combined Effect of ROS Depletion and Calcium Overload Inhibition

A Novel Targeted Nanoparticle for Traumatic Brain Injury Treatment: Combined Effect of ROS Depletion and Calcium Overload Inhibition

  • Adv Healthc Mater. 2022 Jun;11(11):e2102256. doi: 10.1002/adhm.202102256.
Zhengzhong Han 1 2,  Yuhan Han 1,  Xuyang Huang 1 3,  Hongwei Ma 1,  Xuefeng Zhang 1,  Jingyuan Song 4,  Jun Dong 5,  Shanshan Li 6,  Rutong Yu 1 3,  Hongmei Liu 1 2
Affiliations

Affiliations

  • 1 Institute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, 221002, P. R. China.
  • 2 Department of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong, 518055, P. R. China.
  • 3 Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, P. R. China.
  • 4 School of Nursing, Xuzhou Medical University, Xuzhou, 221002, P. R. China.
  • 5 Department of Neurosurgery, the Second Affiliated Hospital of Suzhou University, Suzhou, 215000, China.
  • 6 Jiangsu Medical Engineering Research Center of Gene Detection and Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, 221002, P. R. China.
PMID: 35118827 DOI: 10.1002/adhm.202102256
Abstract

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.

Keywords

Ca2+ influx; lipid-radical scavenger nanoparticles; nimodipine; reactive oxygen species; targeted drug delivery; traumatic brain injury.

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