Histidine Neuroprotective Effect on CA1 Region of Rat Hippocampus Following Transient Brain Ischemia

There are multiple processes that lead to cell death after brain ischemia, such as glutamate release and inflammatory reactions. Histamine is able to suppress inflammatory reactions and glutamate release. Since histidine is precursor of histamine, this study was conducted to evaluate its neuroprotective effects on CA1 region of rat hippocampus following brain ischemia. In the present experimental study, thirty-six male Wistar rats were randomly divided into six groups as the following: control, surgical control, ischemia, and three groups which different doses (200, 500, and 1000 mg/kg) of histidine. Focal cerebral ischemia, for 60 min, was provoked by transient occlusion of the right middle cerebral artery in all groups except the two control groups, and histidine neuro-protective effects on neuronal death was evaluated in CA1 of hippocampus neurons after 7 days. The gathered data was analyzed using one-way ANOVA. The results showed that the mean number of neuronal degeneration and pancellular necrosis in groups which received doses of 500 and 1000 mg/kg of histidine have significantly decreased in comparison with the ischemia group (p=0.001). This reduction in dose of 200 mg/kg of histidine was not statistically significant (p=0.05). Our present findings show that intraperitoneal administration of histidine before reperfusion alleviated CA1 damage.