摘要
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. %26lt;br%26gt;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 degrees C) was imposed for a duration of 2 h. The functional outcome, infarct volume and activated caspase-3 immunoreactivity (IR) were assessed at 8, 24 and 72 h, and one week after the insult. During the experiment the cerebral blood flow (CBF) was measured via Laser Doppler Flowmetry. %26lt;br%26gt;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 h after the Et-1 induced insult and hypothermia significantly reduced the number of apoptotic cells at 8 h, 24 h and 1 week after ischemia. Furthermore, the hypothermic treatment did not affect the CBF in the Et-1 model. %26lt;br%26gt;These findings indicate that in the Et-1 model, hypothermia exerts a long lasting effect on stroke-induced apoptosis.
- 出版日期2013-3-21