Abstract
Topical application of GDNF greatly reduced the infarct size (48%) and brain edema (30%) at 24 hr of continuous MCAO in rats. The reduction of the infarct size was not related to a change of cerebral blood flow (CBF), but was accompanied by marked reduction of positive cells for TUNEL and caspases in the affected area. Thus, GDNF showed a direct protective effect against ischemic brain damage, but not secondary by improving CBF. Based on the strong protective effect of NTF protein against ischemic brain damage and the considerable transfer of a foreign gene into ischemic brain, an adenovirus vector containing the GDNF gene (Ad-GDNF) was prepared, and a possible protective effect of the Ad-GDNF transfer was examined after transient MCAO in rat. Pretreatment of animals with Ad-GDNF 24 hr before the subsequent 90 min of transient MCAO effectively reduced infract volume and area without affecting regional CBF compared to the vehicle or Ad-LacZ animal groups.
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