title: The effects of captopril on lipopolysaccharide induced learning and memory impairments and the brain cytokine levels and oxidative damage in rats.
abstract: OBJECTIVE
  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.
  
  
  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).
  
  
  CONCLUSIONS
  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.
authors: Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Azam
authors: A
authors: Abareshi
authors: Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: hosseinim@mums.ac.ir.
authors: Mahmoud
authors: M
authors: Hosseini
authors: Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Farimah
authors: F
authors: Beheshti
authors: Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Fatemeh
authors: F
authors: Norouzi
authors: Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Majid
authors: M
authors: Khazaei
authors: Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Hamid Reza
authors: HR
authors: Sadeghnia
authors: Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Mohammad Hossein
authors: MH
authors: Boskabady
authors: Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
authors: Mohammad Naser
authors: MN
authors: Shafei
authors: Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.
authors: Akbar
authors: A
authors: Anaeigoudari
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000276:immunology / Q000503:physiopathology; D002216:Captopril / Q000627:therapeutic use*; D016207:Cytokines / Q000276:immunology; D008070:Lipopolysaccharides / Q000009:adverse effects* / Q000276:immunology; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects*; D008569:Memory Disorders / Q000188:drug therapy* / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects; D017208:Rats, Wistar
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D016207:Cytokines; D008070:Lipopolysaccharides; D002216:Captopril
keywords: Captopril; Cytokine levels; Lipopolysaccharide; Memory; Oxidative damage