crocin and Stroke

Intracerebral hemorrhage (ICH) is a devastating subtype of stroke that is associated with high morbidity and mortality. However, up to now, there are no effective prevention methods or specific therapies to improve its clinical outcomes. Herein, we explore preliminarily the efficacy of crocin, a carotenoid extracted from the stigma of saffron known for its anti-oxidation and free radical scavenging activities, in a mouse ICH model induced with collagenase infusion. Crocin or saline was administrated 6 h after ICH and then every 12 h for up to 7 days. Neurological scores were examined on days 1, 3, and 7 after ICH. Mice were sacrificed after1, 3, and 7 days of crocin treatment for examination of histology and immunohistochemistry. The results showed that oral administration of crocin attenuated the neurological deficits and reduced the myelin loss, neuron degeneration, iron deposition, reactive oxygen species (ROS) production and heme oxygenase-1 (HO-1) expression in the early stage of ICH, making it potential to be an ideal candidate for medical therapy of ICH in clinic.

Topics: Animals; Antioxidants; Brain; Brain Edema; Carotenoids; Cerebral Hemorrhage; Collagenases; Disease Models, Animal; Heme Oxygenase-1; Male; Mice; Mice, Inbred C57BL; Nerve Degeneration; Nervous System Diseases; Reactive Oxygen Species; Stroke

Crocin is a water-soluble carotenoid isolated from the Crocus sativus L (saffron) stigma. It has previously been reported that it has protective effects against renal, cardiac, and global cerebral ischemic injury. However its therapeutic effects remain to be clarified regarding ischemic reperfusion injuries, brain edema, and activity of antioxidant enzymes in a transient model of focal cerebral ischemia.. Transient focal cerebral ischemia was induced by 60-minute middle cerebral artery occlusion (MCAO), followed by 23-hour reperfusion. Crocin at doses of 15, 30, 60, and 120 mg/kg intraperitoneally were injected at the start of ischemia. Infarct volume and neurologic outcome were evaluated 24 hours after MCAO. For the therapeutic time window measurement, crocin (60 mg/kg) was given 1, 3, and 6 hours after ischemia; 24 hours later brain edema and antioxidant enzyme activity were assessed.. The results indicated that treatment with crocin at doses of 30, 60, and 120 mg/kg significantly decreased infarct volume by 64%, 74%, and 73%, respectively. Administration of crocin (60 mg/kg) 1 hour before, at the start, or 1 hour after ischemia reduced brain edema by 48%, 52%, and 51%, respectively. Moreover, crocin (60 mg/kg) significantly reduced malondialdehyde (MDA) content and increased activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the ischemic cortex (P< .001).. Our findings indicate that crocin has protective effects against ischemic reperfusion injury and cerebral edema in a rat model of stroke. These effects of crocin may have been exerted primarily by suppression of the production of free radicals and increased antioxidant enzyme activity.

Topics: Animals; Antioxidants; Behavior, Animal; Body Water; Brain; Brain Edema; Brain Ischemia; Carotenoids; Cerebral Infarction; Cerebrovascular Circulation; Dose-Response Relationship, Drug; Glutathione Peroxidase; Male; Malondialdehyde; Rats; Rats, Wistar; Stroke; Superoxide Dismutase; Treatment Outcome