کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8650712 1571135 2018 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Tempol prevents post-traumatic stress disorder induced memory impairment
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی فیزیولوژی
پیش نمایش صفحه اول مقاله
Tempol prevents post-traumatic stress disorder induced memory impairment
چکیده انگلیسی
Post-traumatic stress disorder (PTSD) is a mental health disorder that can develop after a terrifying or life threatening event. Multiple symptoms are noticed in patients with PTSD including cognitive impairment, which was shown to be is associated with oxidative stress. Tempol is a highly efficient membrane-permeable antioxidant. In this study, we investigated the possible protective effect of tempol on PTSD-induced memory impairment. To test this hypothesis, we used single prolonged stress (SPS) model (2 h restrain, 20 min forced swimming, 15 min rest, and 1-2 min diethyl ether exposure) as a model of PTSD. Rats were randomly assigned into four groups: control (provided distilled water), tempol (provided tempol; 80 mg/kg/day by oral gavage for 4 weeks), SPS (exposed to prolonged stress and administered distilled water) and tempol/SPS (exposed to prolonged stress and administered tempol for 4 weeks). We used radial arm water maze to test spatial learning and memory functions and enzyme-linked immunosorbant assay (ELISA) to measure levels of oxidative stress biomarkers in the hippocampus. Results showed that SPS model of PTSD impaired both short and long-term memories (P < 0.05), and chronic tempol administration prevented such effect. Tempol also prevented decreases in hippocampal catalase, and SOD activities, GSH/GSSG ratio and increases TBARS levels, which were all impaired by SPS model of PTSD (P < 0.05). In conclusion, we suggest a protective effect of tempol administration against SPS model of PTSD-induced short- and long- term memory impairment, and we believe that this protective effect of tempol is accomplished, at least partly, through prevention of alternation in oxidative stress in the hippocampus.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Physiology & Behavior - Volume 184, 1 February 2018, Pages 189-195
نویسندگان
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