The effect of gallic acid on oxidative stress parameters and hippocampal cell density in ischemia-renal reperfusion model

Although acute renal injury (AKI) is a consequence of renal ischemia-reperfusion (RIR), RIR-induced oxidative damage also affects distant organs. The aim of this study was to evaluate the effect of gallic acid (GA) on oxidative stress parameters and neuronal density in the brain hippocampus following RIR.

48 male Wistar rats were randomly divided into 4 groups, including control, ischemia/reperfusion+normal saline (RIR+Saline), and ischemia/reperfusion+GA groups at doses of 100 mg/kg (RIR+GA100) and 200 mg/kg (RIR+GA200). Animals in all groups except control underwent unilateral nephrectomy (right). The treatments were performed for 14 days and then, the left kidney was ischemized for 45 minutes. After 72 hours, hippocampal activity levels of catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAC) and malondialdehyde (MDA) were evaluated. Finally, neuronal density was measured in CA1 and CA3 regions of the hippocampus.

A significant decrease in CAT, GPx and TAC and an increase in MDA was observed in RIR + Saline group compared to the control group, which was associated with a significant decrease in neuronal density in CA1/CA3 (p<0.05). While in the GA-treated groups, along with a significant increase in CAT, GPx and TAC and a decrease in MDA in the hippocampus, showed a significant increase in neuronal density of CA1/CA3 regions compared to the RIR+Saline group (p˂0.05).

GA pretreatment can ameliorate oxidative damage and neuronal death in the brain hippocampus of rats with RIR-induced acute renal damage.