| Literature DB >> 26352498 |
Akbar Anaeigoudari1, Mohammad Naser Shafei1, Mohammad Soukhtanloo2, Hamid Reza Sadeghnia3, Parham Reisi4, Farimah Beheshti1, Reza Mohebbati5, Seyed Mojtaba Mousavi5, Mahmoud Hosseini5.
Abstract
Inflammation and oxidative stress have important roles in memory impairment. The effect of 7-nitroindazole (7NI) on lipopolysaccharide (LPS)-induced memory impairment was investigated. Rats were used, divided into four groups that were treated as follows: (1) control (saline); (2) LPS; (3) 7NI-LPS; and (4) 7NI before passive avoidance (PA). In the LPS group, the latency for entering the dark compartment was shorter than in the controls (p < 0.01 and p < 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p < 0.01 and p < 0.001). Malondialdehyde (MDA) and nitric oxide (NO) metabolite concentrations in the brain tissues of the LPS group were higher than in the controls (p < 0.001 and p < 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p < 0.001 and p < 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p < 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p < 0.001). It is suggested that brain tissue oxidative damage and NO elevation have a role in the deleterious effects of LPS on memory retention that are preventable using 7NI.Entities:
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Year: 2015 PMID: 26352498 DOI: 10.1590/0004-282X20150121
Source DB: PubMed Journal: Arq Neuropsiquiatr ISSN: 0004-282X Impact factor: 1.420