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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 &lt; 0.01 and p &lt; 0.001); while in the 7NI-LPS group, it was longer than in the LPS group (p &lt; 0.01 and p &lt; 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 &lt; 0.001 and p &lt; 0.05); while in the 7NI-LPS group, they were lower than in the LPS group (p &lt; 0.001 and p &lt; 0.05, respectively). The thiol content in the brain of the LPS group was lower than in the controls (p &lt; 0.001); while in the 7NI-LPS group, it was higher than in the LPS group (p &lt; 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.

Lipopolysaccharide-induced memory impairment in rats is preventable using 7-nitroindazole