Cerebrovascular disease such as
ischemic stroke develops
cognitive impairment due to brain tissue damage including neural loss,
demyelination and decrease in synaptic density. In the present study, we developed transient
ischemia in the forebrain of the gerbil and found
cognitive impairment using the Barnes maze test and passive avoidance test for spatial memory and learning memory, respectively. In addition, neuronal loss/death was detected in the Cornu Ammonis 1 (CA1) region of the gerbil hippocampus after the
ischemia by
cresyl violet histochemistry, immunohistochemistry for neuronal nuclei and histofluorescence with
Fluoro-Jade B. Furthermore, in the CA1 region following
ischemia, myelin and vesicular synaptic density were significantly decreased using immunohistochemistry for
myelin basic protein and
vesicular glutamate transporter 1. In the gerbils, treatment with COG-up® (a combined extract of Erigeron annuus (L.) Pers. and Brassica oleracea Var.), which was rich in
scutellarin and
sinapic acid, after the
ischemia, significantly improved
ischemia-induced decline in memory function when compared with that shown in gerbils treated with vehicle after the
ischemia. In the CA1 region of these gerbils, COG-up® treatment significantly promoted the remyelination visualized using immunohistochemistry
myelin basic protein, increased oligodendrocytes visualized using a receptor-interacting
protein, and restored the density of glutamatergic synapses visualized using double immunofluorescence for
vesicular glutamate transporter 1 and
microtubule-associated protein, although COG-up® treatment did not protect pyramidal cells (principal neurons) located in the CA1 region form the ischemic insult. Considering the current findings, a gerbil model of
ischemic stroke apparently showed
cognitive impairment accompanied by ischemic injury in the hippocampus; also, COG-up® can be employed for improving
cognitive decline following
ischemia-reperfusion injury in brains.