@article{3123404,
    title = "Silibinin Improves TNF-α and M30 Expression and Histological Parameters in Rat Kidneys After Hepatic Ischemia/Reperfusion",
    author = "Kyriakopoulos, G. and Tsaroucha, A.K. and Valsami, G. and Lambropoulou, M. and Kostomitsopoulos, N. and Christodoulou, E. and Kakazanis, Z. and Anagnostopoulos, C. and Tsalikidis, C. and Simopoulos, C.E.",
    journal = "Journal of Investigative Surgery",
    year = "2018",
    volume = "31",
    number = "3",
    pages = "201-209",
    publisher = "Taylor and Francis Ltd.",
    issn = "0894-1939, 1521-0553",
    doi = "10.1080/08941939.2017.1308044",
    keywords = "silibinin;  tumor necrosis factor;  2 hydroxypropyl beta cyclodextrin;  antioxidant;  cytokeratin 18;  silibinin;  silymarin;  tumor necrosis factor, animal experiment;  animal tissue;  Article;  comparative study;  controlled study;  deterioration;  edema;  filtration;  histology;  histopathology;  hyperemia;  kidney injury;  kidney parenchyma;  kidney tissue;  kidney tubule necrosis;  liver ischemia;  nonhuman;  priority journal;  protein expression;  rat;  reperfusion;  reperfusion injury;  acute kidney failure;  animal;  chemistry;  complication;  disease model;  drug effect;  human;  intravenous drug administration;  kidney;  liver;  male;  metabolism;  necrosis;  pathology;  reperfusion injury;  Silybum marianum;  vascularization;  Wistar rat, 2-Hydroxypropyl-beta-cyclodextrin;  Acute Kidney Injury;  Administration, Intravenous;  Animals;  Antioxidants;  Disease Models, Animal;  Humans;  Keratin-18;  Kidney;  Liver;  Male;  Milk Thistle;  Necrosis;  Rats;  Rats, Wistar;  Reperfusion Injury;  Silymarin;  Tumor Necrosis Factor-alpha",
    abstract = "Background: Remote kidney damage is a sequel of hepatic ischemia–reperfusion (I/R) injury. Silibinin is the main ingredient of the milk thistle plant seed extract with known antioxidant and hepatoprotective activity. Our study investigates the nephroprotective potential of intravenously administered silibinin, as a lyophilized SLB-hydoxypropyl-beta-cyclodextrin product, in hepatic I/R injury. Material and methods: 63 Wistar rats were divided into three groups: Sham (virtual intervention); Control (45 min ischemia and reperfusion); and Silibinin (200 μL intravenous silibinin administration after 45 min of ischemia). Kidney tissues were collected to determine TNF-α, M30 and histopathological changes at predetermined time intervals. Results: Comparing Sham vs. Control groups, proved that hepatic I/R injury increased renal TNF-α and M30 expression. Deterioration was observed in hyperemia/filtration of renal parenchyma and tubules, cortical filtration, tubular necrosis and edema (tissue swelling index). Intravenous silibinin administration and comparison of the Control vs. Silibinin groups showed a statistically significant decrease in TNF-α levels at 240 min following I/R (p < 0.0001), and in M30 at 180 min (p = 0.03) and 240 min (p < 0.0001). Renal parameters have significantly decreased in: hyperemia/filtration of renal parenchyma at 120 min (p = 0.003), 180 min (p = 0.0001) and 240 min (p = 0.0002); hyperemia/filtration of renal tubules at 120 min (p = 0.02), 180 min (p = 0.0001) and 240 min (p = 0.0005); cortical filtration (240 min - p = 0.005); tubular necrosis (240 min - p = 0.021); and edema (240 min - p = 0.001). Conclusion: Our study confirms that hepatic I/R injury causes remote renal damage while the intravenous administration of silibinin leads to statistically significant nephroprotective action. Copyright © 2017 Taylor & Francis Group, LLC."
}