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Cerebral ischemia is a leading cause of death and disability. A previous study indicated that remote ischemic postconditioning (RIP) in the treatment of cerebral ischemia reduces ischemia/reperfusion (I/R) injury. However, the underlying mechanism is not well understood. In the present study, the authors hypothesized that the protective effect of RIP on neurological damage is mediated by exosomes that are released by endothelial cells in femoral arteries. To test this, right middle cerebral artery occlusion/reperfusion with RIP was performed in rats. In addition, an I/R injury cell model was tested that included human umbilical vein endothelial cells (HUVECs) and SH-SY5Y cells. Both the in vivo and in vitro models were examined for injury. Markers of exosomes (CD63, HSP70 and TSG101) were assessed by immunohistochemistry, western blot analysis and flow cytometry. Exosomes were extracted from both animal serum and HUVEC culture medium and identified by electron microscopy. They investigated the role of endothelial cell-derived exosomes in the proliferation, apoptosis, cell cycle, migration and invasion of I/R-injured SH-SY5Y cells. In addition, apoptosis-related molecules caspase-3, Bax and Bcl-2 were detected. RIP was determined to increase the number of exosomes and the expression levels of CD63, HSP70 and TSG101 in plasma, but not in brain hippocampal tissue. The size of exosomes released after I/R in HUVECs was similar to the size of exosomes released in rats subjected to RIP. Endothelial cell-derived exosomes partly suppressed the I/R-induced cell cycle arrest and apoptosis, and inhibited cell proliferation, migration and invasion in SH-SY5Y nerve cells. Endothelial cell-derived exosomes directly protect nerve cells against I/R injury, and are responsible for the protective role of RIP in I/R.

The purpose of the present study was to investigate the expression of matrix metalloproteinase-9 (MMP-9) and interleukin-6 (IL-6) in patients with subarachnoid hemorrhage (SAH) and the clinical significance thereof. Forty-three patients with SAH and 23 healthy individuals were enrolled in this study. Patients were divided into the cerebral vasospasm (CVS) and non-cerebral vasospasm (non-CVS) groups, or the good and poor prognosis groups. Serum levels of MMP-9 and IL-6 were detected by ELISA. Expression levels of MMP-9 and IL-6 mRNAs were detected by RT-qPCR. Expression levels of MMP-9 and IL-6 were elevated with the increase of grades as determined by the Hunt-Hess grading method. Serum levels of MMP-9 and IL-6 in the CVS and poor prognosis groups were significantly higher than those in the control group. Expression levels of MMP-9 and IL-6 in the CVS group were significantly higher than those in the non-CVS group (P