Non-invasive remote ischemic postconditioning stimulates neurogenesis during the recovery phase after cerebral ischemia.

Ischemic postconditioning (IPostC) has been reported to have neuroprotection against ischemic diseases, and one cycle of IPostC induces neurogenesis when treated nearby. To expanding these effects, we explored the effects of repetitively remote IPostC (NRIPostC) on neurogenesis in the subgranular zone (SGZ) and subentricular zone (SVZ) during stroke recovery. Animals underwent transient cerebral ischemia were treated with vehicle or NRIPostC immediately after reperfusion. Neurological severity scores, infarct size, neurogenesis, and protein expression levels of nestin and GFAP were quantified at 3d, 7d, 14d, 21d and 28d post-ischemia. Results showed that NRIPostC significantly reduced acute infarction and improved neurological outcomes during the recovery phase. Meanwhile, NRIPostC significantly increased the number of BrdU+/nestin+ cells in SGZ on day 14 and in the SVZ on days 3, 7 and 14 respectively, and the number of DCX+ cells from days 3 to 14. There were significant increments in the number of BrdU+/NeuN+ and BrdU+/GFAP+ cells in the SGZ and SVZ during the stroke recovery. The changing tendency of the protein expression of nestin and GFAP in DG was consistent with the result mentioned above. In conclusion, NRIPostC reduced acute infarction and improved functional outcomes up to 28d, and it induced neurogenesis both in the SGZ and SVZ.