Grape seed proanthocyanidins (GSP) has been reported to attenuate endoplasmic reticulum (ER) stress-induced apoptosis, which is associated with
ischemic stroke. However, whether GSP pays crucial roles in
ischemic stroke still remains unclear. The purpose of this study is to explore the role of GSP in
ischemic stroke and the underlying mechanism. The
ischemic stroke mouse model was established by
middle cerebral artery occlusion. GSP administration was performed intragastrically. Long-term neurological outcome was assessed by the foot fault test after reperfusion.
Brain injury was identified by
infarct volume from
2,3,5-triphenyltetrazolium chloride staining. Neuronal apoptosis was detected by
terminal deoxynucleotidyl transferase dUTP nick end labeling. The expression levels of Bax, Bcl-2, Cleaved
Caspase-3, phosphorylated ERK (p-ERK), ERK,
Glucose-regulated
protein 78 kDa (
GRP78),
Caspase-12 were detected by western blotting. In mice with
ischemia stroke, GSP administration improved long-term neurological outcomes by attenuating
ischemia-reperfusion induced neuronal apoptosis and
brain injury. Mechanically, GSP performance inhibited the expression levels of ER stress-associated genes. GSP protects mice against
ischemic stroke via attenuating neuronal apoptosis. Moreover, GSP attenuated ER stress-associated apoptosis by inhibiting
GRP78 and
Caspase-12. Our study indicates that GSP attenuates neuronal apoptosis in
ischemic stroke, which shows the potential for
ischemic stroke treatment.