Postconditioning prevents neurologic injury of the spinal cord after ischemia, and the first few minutes of reperfusion are crucial to neuroprotection by postconditioning.

The neuroprotection of exosomes from mesenchymal stem cells on ischemic spinal cords can be enhanced by genetic modification of the exosomes to contain elevated microRNA-25.

Inhibition of miRNA-124 exerts neuroprotection on spinal cords against ischemia-reperfusion injury, possibly by induction of mitophagy and antiapoptotic effects.

Inhibition of miR-320 induces neuroprotection in the spinal cord, against ischemia-reperfusion injury, possibly via up-regulation of phospho-Hsp20.

Overexpression of miRNA-21 exerts neuroprotective effects on spinal cords against ischemia-reperfusion injury, possibly by inhibition of the proapoptotic proteins Faslg and PDCD4.

The two postconditioning methods possess comparable neuroprotective effects on the spinal cord and share a common molecular mechanism, in which phosphatidylinositol 3-kinase and ERK pathways play crucial roles.

: Pretreatment with morphine induces delayed cardioprotection in mice. The authors demonstrated an obligatory role for iNOS in mediating morphine-induced delayed cardioprotection.

No abstract