Ischemic acute kidney injury (AKI) is usually accompanied by neuroinflammation-induced encephalopathy.
However, the specific mechanism remains unclear. Toll-like receptors (TLR), specifically TLR-4 has been linked to
ischemic reperfusion injury in different organs like kidney, brain and liver. Here, we induced an ischemic reperfusion
kidney injury in Sprague Dawley rats. All animals were evaluated using behavioral tests which revealed locomotor
activity and motor disturbances in the AKI group. The brains were then examined by immunostaining with ionized
calcium binding adaptor molecule 1 (microglial marker) and TLR-4 antibodies. The histological analysis revealed
significant up-regulation of TLR-4 in the hippocampus and striatum in the AKI group. These data demonstrate for the first
time, the triggering effect of TLR-4 on AKI-induced neuroinflammation in the brain that may lead to AKI-induced
encephalopathy. This would also generate a novel hypothesis that using TLR blockers may have a role in preventing AKI
effects on the brain.
Keywords: Toll-like receptor-4, acute kidney injury, neuroinflammation, uremic encephalopathy.
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