These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Inhibition of p21-activated kinase 1 by IPA-3 attenuates secondary injury after traumatic brain injury in mice.
    Author: Ji X, Zhang W, Zhang L, Zhang L, Zhang Y, Tang P.
    Journal: Brain Res; 2014 Oct 17; 1585():13-22. PubMed ID: 25148711.
    Abstract:
    The p21-activated kinase 1 (PAK1) is up-regulated in the brain following traumatic brain injury (TBI). Inhibition of PAK1 has been found to alleviate brain edema in a rat model of subarachnoid hemorrhage. Suppressing PAK1 activity might represent a novel therapeutics of attenuating secondary injury following TBI. Here we confirmed that the mRNA and protein levels of PAK1 and the protein level of p-PAK1 were significantly increased after inducing TBI in mice via M.A. Flierl's weight-drop model. A single intraperitoneal administration of IPA-3, a specific PAK1 inhibitor, immediately after TBI significantly reduced the protein level of p-PAK1, cleaved caspase-3 level, the number of apoptotic cells at the lesion sites of TBI mice. It also reduced brain water content and the blood-brain barrier permeability in TBI mice. Furthermore, the administration of IPA-3 significantly reduced the neurological severity score and increased the grip test score in TBI mice. Taken together, we demonstrate that PAK1 inhibition by IPA-3 may attenuate the secondary injury following TBI, suggesting it might be a promising neuroprotective strategy for preventing the development of secondary injury after TBI.
    [Abstract] [Full Text] [Related] [New Search]