Considerable evidence has been accumulated demonstrating an important role for
inflammation in ischemic
brain injury and its contribution to greater cerebral damage after
ischemia. Blocking the inflammatory reaction promotes neuroprotection and shows therapeutic potential for clinical treatment of ischemic
brain injury.
Escin, a natural mixture of
triterpenoid saponin isolated from the seed of the horse chestnut, demonstrates antiedematous and anti-inflammatory effects. Here we assessed
neuroprotective effects of
escin with a transient global
cerebral ischemia model. Global
cerebral ischemia was induced by occluding both common carotid arteries and withdrawing 0.3ml of blood from the tail vein in mice. Treatment with
escin was initiated 0.5h after
ischemia induction and given once a day for three consecutive days. Then animals were assessed using the Morris water-maze test and step-down passive avoidance test.
Acetylcholinesterase (AChE) activity, histological pathology, and expression of inflammatory genes in the hippocampus were determined. The results showed
escin significantly improved learning and memory recovery and reduced hippocampal damage in the cerebral ischemic mice. However,
donepezil merely improved learning and memory recovery but did not ameliorate hippocampal damage in the cerebral ischemic mice. Furthermore, we found
escin significantly downregulated certain inflammatory gene expression and upregulated expression of
granulocyte-macrophage colony-stimulating factor (
GM-CSF), which was recently reported as a neuroprotective
protein in the brain. Our results indicate that inhibition of
inflammation and protection of hippocampal neurons by
escin may be a potentially useful
therapy for ischemic
brain injury.