Aim: Renin-angiotensin system has a role in inflammation and also involves in learning and memory. In the present study, the effects of captopril on lipopolysaccharide (LPS) induced learning and memory impairments, hippocampal cytokine levels and brain tissues oxidative damage was investigated.
Materials and methods: The rats were divided and treated : [1] saline (Control), [2] LPS (1mg/kg), [3-5] 10, 50 or 100mg/kg captopril 30min before LPS. The treatment was started since six days before the behavioral experiments and continued during the behavioral tests (LPS injection two h before each behavioral experiment).
Results: Administration of LPS prolonged the escape latency and traveled path to find the platform in Morris water maze (MWM) test (P<0.01-P<0.001) while, shortened the latency to enter the dark compartment in passive avoidance (PA) test (P<0.001). Pretreatment by all doses of captopril improved performances of the rats in MWM (P<0.05-P<0.001) and also prolonged the latency to enter the dark in PA test (P<0.001). LPS also increased IL-6, TNF-α, malondialdehyde (MDA) and nitric oxide(NO) metabolites in the hippocampal tissues (P<0.05-P<0.001) which were prevented by captopril (P<0.05-P<0.001). The thiol, superoxide dismutase(SOD) and catalase(CAT) in the hippocampus of LPS group were lower than the control (P<0.001) while, they were enhanced when the aniamls were pretraeted by captopril (P<0.01-P<0.001).
Conclusion: The results of present study showed that captopril improved the LPS-induced learning and memory impairments in rats which were accompanied with attenuating hippocampal cytokine levels and improving the brain tissues oxidative damage criteria.
Keywords: Captopril; Cytokine levels; Lipopolysaccharide; Memory; Oxidative damage.
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