Abstract
Transient forebrain or global ischemia induces neuronal death in vulnerable CA1 pyramidal cells with many features. A brief period of ischemia, i.e., ischemic preconditioning, or a modified reperfusion such as ischemic postconditioning, can afford robust protection of CA1 neurons against ischemic challenge. Therefore, we investigated the effect of ischemic preconditioning and postconditioning on neural cell apoptosis in rats. The result showed that both ischemic preconditioning and postconditioning may attenuate the neural cell death and DNA fragment in the hippocampal CA1 region. Further western blot study suggested that ischemic preconditioning and postconditioning down-regulates the protein of cleaved caspase-3, caspase-6, caspase-9 and Bax, but up-regulates the protein Bcl-2. These findings suggest that ischemic preconditioning and postconditioning have a neuroprotective role on global brain ischemia in rats through the same effect on inhibition of apoptosis.
Highlights
Brain ischemia is becoming a leading cause of morbidity and mortality world-wide [1]
We further identified the effect of ischemic preconditioning and postconditioning on neural cell apoptosis and apoptosis-related proteins
We examined whether preconditioning and postconditioning were associated with an increase in neuronal cell survival in the hippocampal CA1 region after ischemia
Summary
Brain ischemia is becoming a leading cause of morbidity and mortality world-wide [1]. The concept of ischemic preconditioning is defined as a brief noninjurious episode of ischemia which can protect the brain from a subsequent longer ischemic insult [10,11] This strategy to attenuate the pathophysiological consequences of ischemic injury would be focused on pretreatment situations, such as protection before bypass surgery. Many researchers demonstrated that a modified reperfusion in the same artery occluded to produce a prolonged episode of focal cerebral ischemia may confer postischemic neuroprotection [12]. Our results showed that ischemic preconditioning and postconditioning have a relatively equal neuroprotective role on global brain ischemia in rats through the same effect on inhibition of neuronal apoptosis
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