Conclusion
CNCbl improves memory impairment following ischemia injury by decreasing neuronal cell death via its antioxidant properties.
Methods
In this experiment, 48 male Wistar rats were selected, which were randomly divided into four groups (n=12 in each group): sham, ischemia/reperfusion, ischemia/reperfusion + CNCbl 200 and 400 (µg/kg). By occlusion of both common carotids, ischemia induction was performed within 20 min. CNCbl at the doses of 200 and 400 µg/kg was injected (IP) at the start of the reperfusion, 24 and 48 hr following reperfusion. The spatial memory was assessed 7 days following ischemia through the Morris water maze test. Antioxidant enzymes, apoptosis, and necrosis were measured after behavioral tests.
Results
CNCbl significantly improved spatial memory impairments (P<0.05), also CNCbl therapy significantly increased both glutathione (P<0.01) and superoxide dismutase (P<0.05) and reduced malondialdehyde (P<0.01) and TNF-α (P<0.05) in comparison with the ischemia group. In addition, CNCbl significantly decreased both apoptosis and necrosis in the hippocampus CA1 (P<0.01).