Quercitrin contributes to the pathogenesis of cerebral
ischemia/reperfusion injury
Since quercitrin impaired GPVI-mediated platelet activation and genetic
and pharmacologic approaches revealed the critical role of GPVI in the
pathogenesis of cerebral ischemia/reperfusion injury,(Stegner, Klaus &
Nieswandt, 2019) we examined the effect of quercitrin using a murine
model of brain injury induced by middle cerebral artery occlusion and
reperfusion. Middle cerebral artery occlusion led to neurological
deficits as assessed using the Neurological deficit score test, as well
as infarction. However, quercitrin (50 or 100 mg/kg, BW)
dose-dependently reduced the infarct volume (Figure 8A and 8B) and
ameliorated neurological behavior disorder (Figure 8C) compared with the
finding in control mice. These results support the protective effects of
quercitrin against stroke-induced brain damage.