Icariside II (IRS) is a metabolite of
icariin, which is derived from Herba
Epimedii. Although the potential
therapeutic effects of
icariin on ischemic
brain injury were well-investigated; the role of IRS in
ischemic stroke is still not addressed clearly. Therefore, the current study aimed to evaluate the effects of IRS on
cerebral ischemia-
reperfusion injury in rats. The rats were pre-treated by IRS (10 or 30 mg kg(-1), twice a day) for 3 days. After pre-treatment, a MCAO (
middle cerebral artery occlusion) for 2 h followed by reperfusion for 24 h was applied on the rats to induce the
cerebral ischemia injury model. The neurological deficit scores were assessed at 24 h after reperfusion, then animals were sacrificed,
infarct volumes were determined by 2,3,5-triphenyltetrazolium chlorid (TTC) staining and
protein expression levels of interleukin-1β (IL-1β), transforming growth factor-β1 (TGF-β1), inhibitory κB (IκB), nuclear factor κB (NF-κB) p65,
peroxisome proliferator-activated receptor α (PPARα), and
peroxisome proliferator-activated receptor γ (PPARγ) were assayed by using Western blot. IRS pretreatment markedly improved the neurological dysfunction and decreased
infarct volume in MCAO rats. In addition, IRS inhibited IL-1β and TGF-β1
protein expression, and resulted in beneficial effects such as inhibition of IκB-α degradation and NF-κB activation induced by MCAO, in a dose-dependent manner. Furthermore, IRS increased the
protein expression levels of PPARα and PPARγ in the ischemic brain. In conclusion, pretreatment with IRS protects against cerebral ischemic/
reperfusion injury via up-regulation of PPARα and PPARγ and inhibition of NF-κB activation.