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).
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.
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.