Abstract

Introduction: Carotid endarterectomy (CEA) is a surgical procedure used in the prevention of ischemic stroke. However, this procedure can cause complications of ischemia-reperfusion injury to the brain. Clusterin (CLU) is a cytoprotective chaperone protein that is released from neurons in response to various neurological injuries. The objective of the study was to report the changes in serum CLU concentrations of patients undergoing CEA.Materials and methods: The study involved 25 patients with severe internal carotid artery stenosis. Serum samples were taken from patients at three different times: within 24 hours preoperatively to CEA, 12 hours postoperatively, and 48 hours postoperatively. Serum CLU concentrations were measured using a commercially available enzyme-linked immunosorbent assay.Results: When compared to concentrations preoperatively, the serum CLU concentration initially decreased during the 12 hours following CEA. However, 48 hours following the procedure there was an increase in the CLU concentration. After statistical analysis, differences were detected in serum CLU concentration between all three recorded measurements (P < 0.05).Conclusion: Data from our study indicate that serum CLU concentrations are affected after CEA. We hypothesize that serum CLU concentrations may depend on brain ischemia-reperfusion injury following this surgical procedure.

Highlights

  • Carotid endarterectomy (CEA) is a surgical procedure used in the prevention of ischemic stroke

  • Data from the study revealed that the serum CLU concentration initially decreased 12 hours after CEA when compared to concentration preoperatively, and increased 48 hours postoperatively

  • Our study revealed that serum CLU concentrations are affected following CEA

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Summary

Introduction

Carotid endarterectomy (CEA) is a surgical procedure used in the prevention of ischemic stroke. Carotid endarterectomy (CEA) is a minimally invasive surgical procedure used in the prevention of ischemic stroke This treatment can cause various complications, including embolism resulting in brain ischemia. Clusterin (CLU) is called apolipoprotein J (ApoJ), sulfated glycoprotein-2, secreted glycoprotein gp, complement lysis inhibitor, testosterone-repressed prostate message 2 (TRPM-2), or complement-associated protein SP40-40 It is found at high concentrations in physiological fluids and is expressed constitutively at variable levels in a wide variety of tissues [3]. CLU is a chaperone protein that has the ability to bind to a wide array of physiological ligands involved in the pathogenesis of Alzheimer’s disease One of these ligands is b-amyloid, for which clusterin mediates clearance from the brain through the blood–brain barrier to the peripheral circulation via megalin [5,17].

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