Synaptic plasticity and cognitive impairment consequences to acute kidney injury: Protective role of ellagic acid

The goal of the current experiment was to define the efficacy and underlying molecular mechanisms of Ellagic acid (EA) on acute kidney injury (AKI) induced impairment in cognitive and synaptic plasticity in rats. 

Administration of 8 ml/kg glycerol (intramuscular) was used to establish the AKI model. Injured animals were treated by EA (25, 50, and 100 mg/kg, daily, gavage) for 14 consecutive days. To approve the renal injuries and the effects of EA on AKI, creatinine values in serum and urea nitrogen (BUN) values in blood were measured. Cognitive performance was investigated using the Morris water maze test. In vivo long-term potentiation (LTP) was recorded from the hippocampus. Then, the level of IL-10β and TNF-α levels were measured using ELISA kits. The integrity index of the Blood-brain barrier (BBB) was assessed by extravasation of Evans blue dye into the brain.

Glycerol injection increased blood urea nitrogen (BUN) and serum creatinine (Scr) levels significantly in the AKI group, and EA treatment resulted in a significant reduction in BUN levels in all concentration groups. Also, a significant reduction in the cerebral EBD concentrations was demonstrated in EA treatment rats. Moreover, the indexes of brain electrophysiology, spatial learning, and memory were improved in the EA administrated group compared with the AKI rats. 

The current experiment demonstrated the efficacy of EA in hippocampal complication and cognitive dysfunction secondary to AKI via alleviating the inflammation.