Abstract
Background and Purpose: Remote ischemic postconditioning (RPostC) is an emerging concept for cerebral infarction protection, and it has better application prospects in clinical practice. However, little is known about the neuroprotection mechanisms of RPostC in cerebral ischemia/reperfusion (I/R) injury. In the present study, we investigated the effects of RPostC on neural cells apoptosis and long-term neurological outcomes in focal cerebral I/R injury in the rat middle cerebral artery occlusion model. Methods: Focal cerebral ischemia was induced by middle cerebral artery occlusion using the intraluminal filament technique in male rats. RPostC was generated by 3 cycles of femoral artery 10-minute occlusion/reperfusion on the right limb at the onset of middle cerebral artery reperfusion. Adult male wistar rats were treated with remote post conditioning after 90 minutes of occlusion (beginning of reperfusion). Infarct volumes were assessed at 24h and 21d of stroke onset. Neurological scores were assessed at 24h and 3d,5d, 7d,10d, 14, 21d after the onset of middle cerebral artery reperfusion. Apoptosis-related molecules were studied at 24h of stroke onset by Western blotting. Results: RPostC treatment up-regulated Bcl-2 and heat-shock protein 70 (HSP70) expression and downregulated Bax expression. RPostC treatment also reduced infarct volumes at 24h and 21d, meanwhile, it also improved the neurologic scores and the long-term neurological outcomes compared with the I/R-only group. Conclusion: These findings indicate that RPostC inhibits focal cerebral I/R injury and improves the neurological outcomes. This neuroprotective effect is likely achieved by anti-apoptotic mechanisms.
Highlights
Brain ischemia is becoming a leading cause of morbidity and mortality world-wide [1]
Regional cerebral blood flow was monitored by laser-Doppler flowmeter with using of a flexible probe over the skull as described earlier [24]. rCBF was measured before ischemia, during MCAO, and during reperfusion
Animals that did not show a CBF reduction of at least 70% were excluded from the experimental group, as well as animals that died after ischemia induction
Summary
Brain ischemia is becoming a leading cause of morbidity and mortality world-wide [1]. Despite extensive researchs on reperfusion injury treatment in the past several decades, few neuroprotectants have been successfully from basic research into clinical application. Innovative treatment strategies for protecting brain against the detrimental effects of this form of injury are required in order to improve clinical outcomes in patients with brain ischemic injury. Researchers are interested in the brain’s endogenous strategies for neuroprotection [6,7]. Harnessing the endogenous protection elicited by the brain’s ability to “condition” itself has recently emerged as a powerful new strategy for limiting brain injury [8,9]. Remote ischemic postconditioning (RPostC) is an emerging concept for cerebral infarction protection, and it has better application prospects in clinical practice. Little is known about the neuroprotection mechanisms of RPostC in cerebral ischemia/reperfusion (I/R) injury. We investigated the effects of RPostC on neural cells apoptosis and long-term neurological outcomes in focal cerebral I/R injury in the rat middle cerebral artery occlusion model
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