Among these studies, human neural progenitor cells isolated from fetal brain have been transplanted into the brain of stroke animal models and found to restore brain function [13], [14].
In stroke animal models, intravenously transplanted human NSCs migrated selectively to the damaged brain sites caused by ischemia and ICH, differentiated into neurons and astrocytes, and promoted functional recovery in these animals [9] [12], [15] [17].
Previous studies have demonstrated that the brain transplantation of human neural stem cells overexpressing VEGF or GDNF in cerebral hemorrhage stroke animal models promoted functional recovery and neuronal protection [45], [46].
Employing a variety of animal models, we have established that deoxygedunin exhibits potent neuroprotective actions in kainic acid neuroexcitotoxicity and stroke animal models (see also Supplemental Materials S1 and Figure S3).
Consistently the reduction of IL-1 beta function, using specific antagonists, results in neuroprotective effects in stroke animal models [ 95].
The mechanisms underlying the improved functional recovery of ischemic stroke animal model subjected to NSCs therapy remain unclear.
