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.