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Year : 2015  |  Volume : 1  |  Issue : 2  |  Page : 159-166

Neural transmission pathways are involved in the neuroprotection induced by post- but not perischemic limb remote conditioning

1 Institute of Hypoxia Medicine, Xuanwu Hospital, Capital Medical University; Center of Stroke, Beijing Institute for Brain Disorder; Beijing Key Laboratory of Hypoxia Translational Medicine, Beijing, China
2 Department of Neurosurgery, Wayne State University School of Medicine, Detroit, Michigan, USA
3 Institute of Hypoxia Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China

Correspondence Address:
Xunming Ji
Institute of Hypoxia Medicine, Capital Medical University, Xuanwu Hospital, Chang Chun Road 45, Beijing - 100 053
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2394-8108.172897

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Background: Remote ischemic preconditioning (PreC) and postconditioning (PostC) have all been shown to be neuroprotective against ischemia/reperfusion (I/R) injury. However, the underlying mechanisms of ischemic perconditioning (PerC) remain largely unknown. This study aimed to investigate the potential role of neural transmission pathways in the transference of protective signals evoked by PerC. Materials and Methods: Male Sprague-Dawley rats were randomly allocated into 12 groups [sham, middle cerebral artery occlusion (MCAO), MCAO+PerC, MCAO+PerC+vehicle, MCAO+PerC+Capsaicin, MCAO+PerC+sham, MCAO+PerC+denervation, MCAO+PostC, MCAO+PostC+vehicle, MCAO+PostC+sham, MCAO+PostC+Capsaicin, MCAO+PerC+denervation]. The I/R model was established by 90-min occlusion of the right middle cerebral artery and subsequent 24 h reperfusion. Remote conditioning was induced with three cycles of 10 min ischemia/10 min reperfusion of the femoral arteries bilaterally. Nerve block was conducted by local capsaicin treatment of exposed nerves or femoral and sciatic nerve transection. Cerebral infarct volumes were quantified by 2, 3, 4-triphenytetrazolium-chloride stain assay. The phosphorylation of Akt was detected by Western blot. Results: Remote ischemic PerC and PostC therapies reduced the infarct size and attenuated neurological deficits. Blocking the neural transmission pathways abolished the protective effect of PostC but had no effect on PerC. Further, blocking the neural transmission pathways reduced periinfarct Akt activation of PostC but had no effect on PerC. Conclusion: Unlike PostC, neural transmission pathways may not play a significant role in the transference of PerC-induced neuroprotection after I/R injury.

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