2026-10-19T01:52:54Zhttps://ebyu-rdlopen.rawdatalibrary.net/oai/requestoai:ebyu-rdlopen.rawdatalibrary.net:ebyu/117822026-10-18T20:34:10Zopenairedrivercom_ebyu_10000col_ebyu_10001Effect of thiamine pyrophosphate on oxidative damage in the brain and heart of rats with experimentally induced occlusion of the common carotid artery.; [Efecto del pirofosfato de tiamina sobre el daño oxidativo en el cerebro y el corazón de ratas con oclusión inducida experimentalmente de la arteria carótida común.]Emir, IzzetSuleyman, ZeynepSuleyman, Haliscarotid arteryıschemiaocclusionratreperfusionthiamine pyrophosphatecocarboxylasecreatine kinasecytokineglutathioneinterleukin 1betainterleukin 6ketamineliquid nitrogenmalonaldehydepyrophosphatethiobarbituric acid reactive substancetroponin Itumor necrosis factoranesthesiaanimal modelanimal tissueArticleblood brain barrierbrain blood flowcommon carotid arterynonhumanoxidative stressrevascularizationsham procedureIt is known that a sudden increase in cerebral blood flow (hyperper-fusion) with carotid revascularisation may disrupt and damage the blood-brain barrier. This study aimed to explore thiamine pyrophosphate’s (TPP) protective effects against potential brain and heart damage resulting from carotid cross-clamping and unclamping in rats. The animals were divided into common carotid cross-clamping and unclamping (CCU), TPP+common carotid cross-clamping and unclamping (TCCU), and sham operation (SG) groups. The TCCU group received an intraperitoneal injection (IP) of 20 mg/kg TPP one hour before anesthesia. The CCU and SG groups received distilled water as a solvent. Ischemia was induced by maintaining the clips closed for 10 min. For the SG group, only a subcutaneous incision was made. Afterward, the clips were removed, the incisions were stitched, and reperfusion was continued for six hours. Subsequently, the rats were euthanized with high-dosage general anesthesia, and heart and brain tissues were removed. TPP significantly suppressed the I/R-induced malondialdehyde (MDA) increase and decreased total glutathione (tGSH) levels in brain and heart tissues. TPP prevented the increase of tumor necrosis factor-alpha (TNF-α), interleukin-1 β (IL-1β), and interleukin-6 (IL-6) levels in both brain and heart tissues. In blood serum, TPP suppressed I/R-induced increase in troponin I (TP I) and creatine kinase-MB (CK-MB) in the blood. TPP was shown to protect the brain and distant cardiac tissues against oxidative and inflammatory damage induced by cerebral I/R. © 2024, Instituto de Investigaciones Clinicas. All rights reserved.Instituto de Investigaciones Clinicas2024Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/11782https://doi.org/10.54817/ic.v65n2a080535-5133enInvestigacion Clinica (Venezuela)info:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/11782