Xianli Meng, Yuejuan Li, Jian Zhang, Xiaofeng Jiang, Xiangyang Tian and Jianhua Zhao
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.