Adamantios Michalinos1, Alexandra K Tsaroucha1,2, Maria Lambropoulou3, Dimitrios Schizas1,4, Georgia Valsami5, Nikolaos Kostomitsopoulos6, Michael S Pitiakoudis1,2, Constantinos E Simopoulos1,2. 1. Postgraduate Program in Hepatobiliary/Pancreatic Surgery, Democritus University of Thrace, Alexandroupolis, Greece. 2. 2nd Department of Surgery and Laboratory of Experimental Surgery, Democritus University of Thrace, Alexandroupolis, Greece. 3. Laboratory of Histology-Embryology, Faculty of Medicine, Democritus University of Thrace, Alexandroupolis, Greece. 4. First Department of Surgery, National and Kapodistrian University of Athens, Athens, Greece. 5. School of Health Sciences, Department of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece. 6. Department of Experimental Surgery, Bioresearch Foundation of the Academy of Athens, Athens, Greece.
Abstract
BACKGROUND: Glycoprotein non-metastatic melanoma B (GPNMB) is a transmembrane glycoprotein with various roles in inflammation regulation, tissue remodeling and oncogenesis. Clinical situations implicating alterations in its expression include ischemic injury, cirrhosis and fatty liver disease amongst other. We examine its expression in hepatic and renal tissue following hepatic ischemia-reperfusion (I/R) in a rat model, with and without intravenous silibinin administration, as a silibinin-hydroxypropyl-β-cyclodextrin lyophilized complex (SLB-HP-β-CD). METHODS: Sixty-three Wistar rats were divided into 3 groups: sham group (virtual intervention; 7 animals), control (C) group (45 min of ischemia, followed by reperfusion and euthanasia at 60, 120, 180 and 240 min; 28 animals equally divided), and silibinin (Si) group (45 min of ischemia, intravenous administration of SLB-HP-β-CD, reperfusion and euthanasia at the same time points; 28 animals equally divided). GPNMB expression was examined in liver and kidney tissue. RESULTS: GPNMB expression was significantly increased following hepatic I/R in the control group, in kidney tissue, in a time dependent manner. In the silibinin group, GPNMB expression significantly decreased with time compared to the control group in both liver and kidney tissue (P<0.05). CONCLUSIONS: Hepatic I/R causes increase of GPNMB levels both in liver and kidney tissues, which may reflect tissue injury. Silibinin seems to act protectively on both liver and kidney, and can be potentially used as a therapeutic approach against hepatic I/R injury. 2020 Translational Gastroenterology and Hepatology. All rights reserved.
BACKGROUND: Glycoprotein non-metastatic melanoma B (GPNMB) is a transmembrane glycoprotein with various roles in inflammation regulation, tissue remodeling and oncogenesis. Clinical situations implicating alterations in its expression include ischemic injury, cirrhosis and fatty liver disease amongst other. We examine its expression in hepatic and renal tissue following hepatic ischemia-reperfusion (I/R) in a rat model, with and without intravenous silibinin administration, as a silibinin-hydroxypropyl-β-cyclodextrin lyophilized complex (SLB-HP-β-CD). METHODS: Sixty-three Wistar rats were divided into 3 groups: sham group (virtual intervention; 7 animals), control (C) group (45 min of ischemia, followed by reperfusion and euthanasia at 60, 120, 180 and 240 min; 28 animals equally divided), and silibinin (Si) group (45 min of ischemia, intravenous administration of SLB-HP-β-CD, reperfusion and euthanasia at the same time points; 28 animals equally divided). GPNMB expression was examined in liver and kidney tissue. RESULTS: GPNMB expression was significantly increased following hepatic I/R in the control group, in kidney tissue, in a time dependent manner. In the silibinin group, GPNMB expression significantly decreased with time compared to the control group in both liver and kidney tissue (P<0.05). CONCLUSIONS: Hepatic I/R causes increase of GPNMB levels both in liver and kidney tissues, which may reflect tissue injury. Silibinin seems to act protectively on both liver and kidney, and can be potentially used as a therapeutic approach against hepatic I/R injury. 2020 Translational Gastroenterology and Hepatology. All rights reserved.
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