The Effects of Exercise on Cortical Oxidative Stress Markers and Memory Impairments Induced by Lipopolysaccharide in Rats

Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
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NIMED03_046

تاریخ نمایه سازی: 7 آبان 1398

Abstract:

Lipopolysaccharide (LPS) is a potent bacterial endotoxin derived from the cell wall of gramnegative bacteria, and neuroinflammation inducedby LPS administration is a common animal model of Alzheimer’s disease (AD). Physical exercise has an effective role to improve eurodegenerative diseases. In this study, the exercise effects on behavioral tests and cortical oxidative stress of lipopolysaccharide(LPS) administered rats were investigated. Materials and Methods: The rats were divided into four groups (N=8): (1) control; (2) moderate training (MT, 15 m/ min, 30 min/day, 9 weeks); (3) LPS (1 mg/kg LPS) and (4) LPS+MT (1 mg/kg LPS; 15 m/min, 30 min/day, 9 weeks). LPS was injected two hours before the behavioral experiments during the last week of training. Finally, the rats’ brain were removed for biochemical assessments. Results: LPS increased escape latency and traveled distance to reach the platform as well as decreased the time spend and traveled distance in target quadrant of Morris water maze (MWM) test (P<0.05-P<0.001). In the passive avoidance (PA) test, LPS decreased the latency to enter the dark compartment and the time spent in the light compartment and increased the time spent in the dark compartment (P<0.01-P<0.001), while MT improved the rats performances in MWM and PA tests (P<0.01-P<0.001). Additionally, LPS increased malondialdehyde (MDA) and nitric oxide metabolite, and decreased thiol contents and catalase (CAT) and superoxide dismutase (SOD) activity in the cortical tissues compared to the control group (P<0.01-P<0.001);while moderate training decreased the levels of MDA;increased thiol contents and SOD and CAT activity in the LPS+MT compared to the LPS group (P<0.001). Conclusion: These results indicated that moderate training improved LPS-induced learning and memory impairments by attenuating the brain oxidative damage.

Authors

Zahra Jahangiri

Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

Zahra Gholamnezhad

Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

Mahmoud Hosseini

Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran