Abstract: Objective: To study the protective effects of emodin on the memory of mice experiencing cerebral ischemia reperfusion and their underlying mechanisms. Methods: Using improved Himori method, cerebral ischemia reperfusion injury was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. The protective effects of emodin (10.0, 1.0, 0.1 mg.kg^-1，ip) on the memory of these mice were examined using the step-through test, shuttle box test,  antihypoxia test under normal pressure, test of acute cerebral hypoxia induced by decapitated mice and test of NaNO₂ histotoxic anoxia,. Meanwhile, the superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-PX) activity were also measured. Results: Emodin could attenuate the memory impairment induced by cerebral ischemia reperfusion injury, prolong the antihypoxic survival time, and increase the activities of GSH-PX and SOD. Conclusions: Emodin showed protective effects on the memory of mice with cerebral ischemia reperfusion injury. The possible mechanism may involve the enhancement of the activities of GSH-PX and SOD, which leads to the increased oxygen free radicals scavenging ability, enforced antihypoxic capacity and alleviation of cerebral ischemia damage.

Key words: emodin, cerebral ischemia reperfusion, learning and memory, oxygen free radicals, antihypoxia