Mild hypothermia reduces activated caspase-3 up to 1 week after a focal cerebral ischemia induced by endothelin-1 in rats

Tine Zgavc, Deborah De Geyter, An-Gaelle Ceulemans, Wendy Stoop, Said Hachimi-Idrissi, Yvette Michotte, Sophie Sarre, Ron Kooijman

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)

Abstract

Abstract: Hypothermia is a promising neuroprotective therapy that has been shown to reduce
apoptosis after an ischemic insult. This study evaluated the effect of mild hypothermia on activated
caspase-3 up to 1 week after the induction of a stroke.
Endothelin-1 (Et-1) was used to elicit transient focal cerebral ischemia in rats. Twenty minutes after
the ischemic insult, a state of mild hypothermia (33°C) was imposed for a duration of two hours. The
functional outcome, infarct volume and activated caspase-3 immunoreactivity (IR) were assessed at 8,
24 and 72 hours, and one week after the insult. During the experiment the cerebral blood flow (CBF)
was measured via Laser Doppler Flowmetry.
Hypothermia improved the neurological outcome at all of the time points studied compared to the
normothermic group, and was associated with a reduction in infarct volume. In both groups, activated
caspase-3 IR peaked 24 hours after the Et-1 induced insult and hypothermia significantly reduced the
number of apoptotic cells at 8 hours, 24 hours and 1 week after ischemia. Furthermore, the
hypothermic treatment did not affect the CBF in the Et-1 model.
These findings indicate that in the Et-1 model, hypothermia exerts a long lasting effect on strokeinduced
apoptosis.
Original languageEnglish
Pages (from-to)81-88
JournalBrain Research
Volume1501
Publication statusPublished - 2013

Keywords

  • Ischemic stroke
  • hypothermia
  • apoptosis

Fingerprint

Dive into the research topics of 'Mild hypothermia reduces activated caspase-3 up to 1 week after a focal cerebral ischemia induced by endothelin-1 in rats'. Together they form a unique fingerprint.

Cite this