Geldanamycin reduced brain injury in mouse model of intracerebral hemorrhage

Anatol Manaenko, Nancy Fathali, Shammah Williams, Tim Lekic, John H. Zhang, Jiping Tang

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

We investigated the effect of the heat shock protein inducer geldanamycin on the development of secondary brain injury after ICH in mice. The effect of the drug at two different concentrations was evaluated at two time points: 24 and 72 h after ICH induction. In the first part of this study, a total of 30 male CD-1 mice were randomly divided into four groups: one sham group and three ICH groups. ICH animals received either an intraperitoneal injection of vehicle or geldanamycin (1 or 10 mg/kg). Neurological deficits and brain water content were evaluated 24 h after ICH. In the second part of this study, the effect of a high concentration of geldanamycin was evaluated 72 h after ICH. Neurological deficits were evaluated by the Garcia neuroscoring, wire hanging and beam balance tests. For estimation of brain water content, the "wet/dry weight" method was used. We demonstrated that administration of geldanamycin (10 mg/kg) ameliorated ICH-induced increase of brain water content significantly in both parts of the study. Geldanamycin improved the neurological outcome according to performance on Garcia and beam balance tests in the 72 h part of this study. Geldanamycin-induced induction of heat shock protein after ICH has a neuroprotective effect and may be a therapeutic target for ICH.

Original languageEnglish
Title of host publicationIntracerebral Hemorrhage Research
Subtitle of host publicationFrom Bench to Bedside
PublisherSpringer-Verlag Wien
Pages161-165
Number of pages5
Edition111
ISBN (Print)9783709106921
DOIs
StatePublished - 2011

Publication series

NameActa Neurochirurgica, Supplementum
Number111
ISSN (Print)0065-1419
ISSN (Electronic)0001-6268

ASJC Scopus Subject Areas

  • Surgery
  • Clinical Neurology

Keywords

  • Geldanamycin
  • HSP
  • ICH
  • Neuroprotection

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