Hydroxy Yellow A Against Brain Ischemic Efficacy And Mechanism Of Action Research

Hydroxysafflor yellow A was extracted as a pure component from Carthamus tinctorius L. The present study was designed to document the effects of hydroxysafflor yellow A on cerebral ischemic injuries in rats, and investigate its mechanisms of anti-cerebral ischemic injuries.We validated its protective effects against cerebral ischemic injuries in three different cerebral ischemic models in rats: focal cerebral ischemia-reperfusion was induced by the origin of MCA occlusion with a nylon suture, permanent focal cerebral ischemia induced by electrocoagulation of the middle cerebral artery, global cerebral ischemia-reperfusion induced by four-artery-occlusion. The results showed Hydroxysafflor Yellow A effectively improved the abnormal neurological deficits and reduced the infarct rate and protected from focal cerebral ischemia/reperfusion injuries. In global cerebral ischemic experiments, we found Hydroxysafflor Yellow A significantly prolonged EEG disappearing time, shortened righting reflex and electroencephalogram recovering time with a concomitant decreased the water content of brain tissue.In studying anti- cerebral ischemic mechanisms of hydroxysafflor yellow A, the results showed that hydroxysafflor yellow A reduced the whole blood viscosity, inhibited AA-induced platelet aggregation and protected neuron cells from damage induced by anoxia-reoxygenation or glutamic acid, but had no effect on the plasma viscosity, the amount of fibrinogen and the activity of plasmin. It has also been shown that, hydroxysafflor yellow A decreased the percentage of the apoptotic neuron cells, and inhibited the expression of inducible nitric oxide synthase(iNOS) which increased during the process of cerebral ischemia.In conclusion, all the data indicate that hydroxysafflor yellow A has protective effects against cerebral ischemia injuries in rats and its anti-cerebral ischemia effects through reducing the blood viscosity and inhibiting platelet aggregation, decreasing the apoptosis and inhibiting the expression of iNOS.