Silibinin Improves TNF-alpha and M30 Expression and Histological Parameters in Rat Kidneys After Hepatic Ischemia/Reperfusion

摘要

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 (45min ischemia and reperfusion); and Silibinin (200 L intravenous silibinin administration after 45min of ischemia). Kidney tissues were collected to determine TNF-, M30 and histopathological changes at predetermined time intervals. Results: Comparing Sham vs. Control groups, proved that hepatic I/R injury increased renal TNF- 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- levels at 240min following I/R (p 0.0001), and in M30 at 180min (p = 0.03) and 240min (p 0.0001). Renal parameters have significantly decreased in: hyperemia/filtration of renal parenchyma at 120min (p = 0.003), 180min (p = 0.0001) and 240min (p = 0.0002); hyperemia/filtration of renal tubules at 120min (p = 0.02), 180min (p = 0.0001) and 240min (p = 0.0005); cortical filtration (240min - p = 0.005); tubular necrosis (240min - p = 0.021); and edema (240min - 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.