Neuroprotective effect of lutein in diabetic mice after ischemia/reperfusion injury

Abstract

Purpose: Stroke is a major cause of death and is more prevalent in diabetic patients. Our previous studies showed lutein’s neuroprotective effect against ischemia/reperfusion (I/R) injury. The aim of this study is to identify the potential of lutein in protecting the brain and retina from I/R injury under diabetic condition. Methods: Male Ins2Akita/+ diabetic mice were used. Under gas anesthesia, the middle cerebral artery (MCA) was occluded by inserting a coated filament from the external carotid artery through the internal carotid artery. Successful occlusion of MCA was verified by laser-Doppler measurment of relative cerebral blood flow in the MCA territory. After two hours of occlusion the filament was withdrawn to allow reperfusion. 0.2 mg/kg lutein was administrated intraperitoneally one hour before and after reperfusion. Following neurological score assessment and the electroretinogram (ERG) recording, brain slices were collected and stained with triphenyltetrazolium chloride. The size of infract, hemispheric swelling and hemorrhage transformation were measured. Results: Lutein treatment increased the survival rate of diabetic Ins2Akita/+ mice after I/R injury. Around 20% vehicle-treated animals died before collection while 100% lutein-treated animals survived. More importantly, for the ones that survived, lutein treatment showed a significant decrease in neurological score. However, there was minimal improvement in infarct area, infarct volume and ERG recordings while hemispheric swelling was slightly decreased after lutein treatment. Conclusions: A better neurological outcome in diabetic mice after lutein treatment suggests a decrease in severity of neurological deficits, indicating the potential of lutein as a neuroprotective agent against ischemia/reperfusion injury under diabetic condition.