ABSTRACT
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.
Acknowledgments
The authors would like to thank the National Institute for Medical Research Development (Grant No: 971287) for its financial support.
Data availability
The data used to support the findings of this study are available from the corresponding author upon request.
Conflicts of interest
There is no conflict of interest.