Osteopontin (OPN) is a phosphorylated glycoprotein, which is a soluble cytokine capable of stimulating signal transduction pathways in many different types of cells [12–14]. OPN is up-regulated in the post-ischemic brain [15,16] and plays a protective role due to its anti-inflammatory, neurogenic and nerve guidance effects [17–19]. OPN was induced in a delayed manner in stroke animal models [15,16], beginning from 24 h and peaking at 5 days; however, supplementing OPN during the early period substantially suppressed infarct formation and mitigated neuronal damage [20,21], indicating a more active role of OPN in a hyperacute period of post-ischemic brain.
To understand the optimal effects of GMS-mediated drug delivery in pathological brains, it is critical to ensure a pathology-reflected delivery of encapsulated protein in the pathological brains. This study was undertaken to examine the neuroprotective efficacy of recombinant human OPN encapsulated in GMSs in a rat model of focal cerebral ischemia. In addition, we presented the degradation profiles of GMSs in the normal and post-ischemic brain as determined using scanning electron micrographs, and the actual amounts of OPN released from GMSs into the parenchyma of normal and ischemic brain, demonstrating the usefulness of GMSs to elaborate the neuroprotective potency of OPN in the post-ischemic brain in a hyperacute period.