Abstract
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.
CNS & Neurological Disorders - Drug Targets
Title:Up-Regulation of TLR-4 in the Brain After Ischemic Kidney-Induced Encephalopathy in the Rat
Volume: 12 Issue: 5
Author(s): Mohamed Salama, Sally Mohamed Farrag, Sarah abulfath abulasrar, Maha Mohamed Amin, Azza Abdel-Aziz Ali, Hussein Sheashaa, Mohamed Sobh and Oscar Arias-Carrion
Affiliation:
Keywords: Toll-like receptor-4, acute kidney injury, neuroinflammation, uremic encephalopathy.
Abstract: 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.
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Cite this article as:
Salama Mohamed, Farrag Mohamed Sally, abulasrar abulfath Sarah, Amin Mohamed Maha, Ali Abdel-Aziz Azza, Sheashaa Hussein, Sobh Mohamed and Arias-Carrion Oscar, Up-Regulation of TLR-4 in the Brain After Ischemic Kidney-Induced Encephalopathy in the Rat, CNS & Neurological Disorders - Drug Targets 2013; 12 (5) . https://dx.doi.org/10.2174/1871527311312050006
DOI https://dx.doi.org/10.2174/1871527311312050006 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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