Study summary · research use only
Neuroprotective action of Cortexin, Cerebrolysin and Actovegin in acute or chronic brain ischemia in rats
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, researchers compared Cortexin, Cerebrolysin, and Actovegin in models of acute (middle cerebral artery occlusion) and chronic (common carotid artery stenosis) brain ischemia in male rats, dosed for 10 days at 1 or 3 mg/kg/day (Cortexin), 538 or 1614 mg/kg/day (Cerebrolysin), and 200 mg/kg/day (Actovegin). Using behavioral tests and brain analysis, Cortexin and Cerebrolysin, and to a lesser extent Actovegin, were associated with recovery of neurological function and reduced sensorimotor and cognitive impairment; Cortexin also reduced necrosis in acute ischemia and improved antioxidant activity in chronic ischemia. Radiolabeled Cortexin crossed the blood-brain barrier in mice at 6-8% of blood concentrations, and in vitro assays showed Cortexin bound AMPA (80.1%), kainate (73.5%), mGluR1 (49.0%), GABAA1 (44.0%), and mGluR5 (39.7%) receptors at 10 μg/ml.
Abstract
This study was the first to compare the neuroprotective activity of Cerebrolysin®, Actovegin® and Cortexin® in rodent models of acute and chronic brain ischemia. The neuroprotective action was evaluated in animals with acute (middle cerebral artery occlusion) or chronic (common carotid artery stenosis) brain ischemia models in male rats. Cortexin® (1 or 3 mg/kg/day), Cerebrolysin® (538 or 1614 mg/kg/day) and Actovegin® (200 mg/kg/day) were administered for 10 days. To assess the neurological and motor impairments, open field test, adhesive removal test, rotarod performance test and Morris water maze test were performed. Brain damage was assessed macro- and microscopically, and antioxidant system activity was measured in brain homogenates. In separate experiments in vitro binding of Cortexin® to a wide panel of receptors was assessed, and blood-brain barrier permeability of Cortexin® was assessed in mice in vivo. Cortexin® or Cerebrolysin® and, to a lesser extent, Actovegin® improved the recovery of neurological functions, reduced the severity of sensorimotor and cognitive impairments in rats. Cortexin® reduced the size of necrosis of brain tissue in acute ischemia, improved functioning of the antioxidant system and prevented the development of severe neurodegenerative changes in chronic ischemia model. Radioactively labeled Cortexin® crossed the blood-brain barrier in mice in vivo with concentrations equal to 6-8% of concentrations found in whole blood. During in vitro binding assay Cortexin® (10 μg/ml) demonstrated high or moderate binding to AMPA-receptors (80.1%), kainate receptors (73.5%), mGluR1 (49.0%), GABAA1 (44.0%) and mGluR5 (39.7%), which means that effects observed in vivo could be related on the glutamatergic and GABAergic actions of Cortexin®. Thus, Cortexin, 1 or 3 mg/kg, or Cerebrolysin®, 538 or 1614 mg/kg, were effective in models acute and chronic brain ischemia in rats. Cortexin® contains compounds acting on AMPA, kainate, mGluR1, GABAA1 and mGluR5 receptors in vitro, and readily crosses the blood-brain barrier in mice.
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