ArticleTranslational gastroenterology and hepatology2020
Glycoprotein non-metastatic melanoma B expression after hepatic ischemia reperfusion and the effect of silibinin.
Article in Translational gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Isosteviol plays a protective role on hepatic ischemia and reperfusion injury in mice through MAPK/NF-κB signaling pathway.Translational gastroenterology and hepatology · 2024Article
- Immature tertiary lymphoid structure formation was increased in the melanoma tumor microenvironment ofTranslational cancer research · 2022Article
- Mechanism of hydroxysafflor yellow A on acute liver injury based on transcriptomics.Frontiers in pharmacology · 2022Article
- The Role of GPNMB in Inflammation.Frontiers in immunology · 2021Review
- Use of natural anti-oxidants in experimental animal models of hepatic ischemia-reperfusion injury.Annals of medicine and surgery (2012) · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycoprotein 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).
methodsSixty-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.
resultsGPNMB 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).
conclusionsHepatic 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.
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