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The effect of the brain-derived neurotrophic factor (BDNF), cytokines, and renin angiotensin system (RAS) on memory function have been demonstrated. In this study, the effects of RAS inhibitor captopril (Capto) on hippocampal BDNF, interleukin −6 (IL-6), oxidative stress indicators, and nitric oxide (NO) in scopolamine (Sco)-induced memory impairment in rats were examined. The groups were (1) control, (2) Sco in which Sco was applied 30 min prior to the behavioral tests, and (3–5) Sco-Capto 10, 50, and 100 groups, where Capto (10, 50, or 100 mg/kg), were applied 2 weeks prior to the experiment, as well as 30 min prior to each Sco injection. The Morris Water Maze (MWM) test was conducted, and BDNF, IL-6, NO metabolites, malondialdehyde (MDA), thiol, superoxide dismutase (SOD), and catalase (CAT) were measured. Sco increased the delay and distance to the platform in the MWM test (P <.01 to P <.001), while shortening the time and distance in the target area (P <.01 to P <.001). Additionally, Sco increased IL-6, NO metabolites, and MDA, while decreasing BDNF, thiol, SOD, and CAT (P <.01 to P <.001). Although the Capto reduced the latency and distance traveled to the platform (P <.05 to P <.001), it elevated the time and distance traveled in the target area (P <.05 to P <.01). Furthermore, Capto improved BDNF, thiol, SOD, and CAT levels, and decreased IL-6, NO metabolites, and MDA (P <.05 to P <.001). RAS has a role in learning and memory impairment due to cholinergic system dysfunction. The possible mechanism(s) are including its effects on BDNF, neuro-inflammation and oxidative stress. [ABSTRACT FROM AUTHOR]

Introduction: Angiotensin converting enzyme (ACE) inhibitors are suggested to have some beneficial effects on the brain. In the present study the protective effects against brain tissues oxidative damage as possible mechanism for learning and memory improving effects of captopril was investigated in scopolamine treated rats. Methods: Fifty male Wistar rats were divided into seven groups and treated: saline as a control group, Sco (scopolamine) and Sco-Capto10, 50 and 100 (captopril 10, 50 and 100mg/kg before scopolamine). Treatment was passive avoidance test and then the cortical tissues were collected to measure malondialdehyde (MDA), nitric oxide (NO) metabolites, thiol, super oxide dismutase (SOD) and catalase (CAT). Results: Scopolamine decreased the latency to enter the dark in passive avoidance test compared to control group. It also increased MDA and NO metabolites while decreased thiol, SOD and CAT in comparison with control group. Captopril increased the latency to enter the dark. It also decreased MDA and NO metabolites while, increased thiol, SOD and CAT. Conclusion: Captopril protected brain tissues oxidative damage and improved learning and memory impairment induced by scopolamine. [ABSTRACT FROM AUTHOR]