The leaf extract of Platycarya strobilacea (PSL) has long been recognized as possessing various health-promoting activities. However, information on its possible protective effects against
ischemic stroke is currently lacking. Here, using a mouse model of focal
cerebral ischemia (fCI), we studied the protective potential of an oral supplement of PSL. Mice were randomly divided into four groups: SO, a group subjected to a
sham-operation; VEH, pretreated with distilled water and subjected to
middle cerebral artery occlusion and reperfusion (MCAO/R); PSL-L and PSL-H, pretreated with low (20 mg/kg) and high (100 mg/kg) doses of PSL, respectively, and subjected to the MCAO/R procedure. PSL was administered via an oral route daily for 8 days prior to surgery. We then measured the
infarct volumes and sensorimotor deficits and studied the underlying
antioxidant mechanisms by quantifying apoptosis,
reactive oxygen species (ROS) generation, oxidative damages, and
antioxidant enzymes in the ischemic cortex. The results showed a marked attenuation in
infarct volume and sensorimotor deficits in both the PSL-L and PSL-H groups when compared with VEH. The
terminal deoxynucleotidyl transferase dUTP nick end labeling and the immunohistochemical detection of the cleaved
caspase-3 revealed that PSL could reduce cellular apoptosis in the ischemic lesion in a dose-dependent manner. The
dihydroethidium-fluorescence,
4-hydroxynonenal, and 8-hydroxyl-2'-deoxyguanosine immunoreactivities in the ischemic lesion were markedly attenuated in the PSL-L group compared with the VEH group, indicating that PSL could attenuate ROS generation and the associated oxidative damage in the ischemic cortex. Finally, western blot results indicated that PSL can upregulate levels of
heme oxygenase-1 (HO-1), an
antioxidant enzyme, in the lesion area. Together, these results suggest that PSL can exert protective effects against fCI, and the mechanism may involve HO-1 upregulation.