Sulforaphane decreases kidney injury after transplantation in rats

• Verfasst von: Cekauskas, Albertas [VerfasserIn]
• Verfasst von: Bruns, Helge [VerfasserIn]
• Verfasst von: Manikas, Martynas [VerfasserIn]
• Verfasst von: Herr, Ingrid [VerfasserIn]
• Verfasst von: Groß-Weissmann, Marie-Luise [VerfasserIn]
• Verfasst von: Zorn, Markus [VerfasserIn]
• Verfasst von: Jankevicius, Feliksas [VerfasserIn]
• Verfasst von: Strupas, Kestutis [VerfasserIn]
• Verfasst von: Schemmer, Peter [VerfasserIn]
• Titel: Sulforaphane decreases kidney injury after transplantation in rats
• Titelzusatz: role of mitochondrial damage
• Verf.angabe: Albertas Cekauskas, Helge Bruns, Martynas Manikas, Ingrid Herr, Marie-Luise Gross, Markus Zorn, Feliksas Jankevicius, Kestutis Strupas, Peter Schemmer
• E-Jahr: 2013
• Jahr: 2013.09.18
• Umfang: 9 S.
• Teil: volume:18
• Teil: year:2013
• Teil: pages:488-496
• Teil: extent:9
• Fussnoten: Gesehen am 18.03.2021
• Titel Quelle: Enthalten in: Annals of transplantation
• Ort Quelle: Warsaw, 1996
• Jahr Quelle: 2013
• Band/Heft Quelle: 18(2013), Seite 488-496
• ISSN Quelle: 1425-9524
• DOI: doi:10.12659/AOT.884013
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Animals
• Sach-SW: Antioxidants
• Sach-SW: Apoptosis
• Sach-SW: Isothiocyanates
• Sach-SW: Kidney
• Sach-SW: Kidney Transplantation
• Sach-SW: Male
• Sach-SW: Mitochondria
• Sach-SW: Rats
• Sach-SW: Reperfusion Injury
• Sach-SW: Superoxide Dismutase
• K10plus-PPN: 1751707873

Abstract

BACKGROUND: Sulforaphane is a naturally occuring antioxidative and anti-inflammatory isothiocyanat. In this study, its impact on experimental kidney transplantation was evaluated. - MATERIAL AND METHODS: Male Brown Norway rats (n=112) were used as experimental animals. Donor kidneys were harvested and stored for 12 hours in HTK-solution at 4°C. D,L-Sulforaphane (4.4 mg/kg BW; 0.2ml) or normal saline (0.2 ml) was given i.v. to the recipients 24 and 1 hour before, and 6 hours after transplantation. Recipients were nephrectomized bilaterally and subsequently transplantation was performed. After 6 and 48 hours, biopsies were taken and processed for light and electron microscopy. Graft function was monitored using serum values of creatinine and BUN after 6 and 24 hours. Quantitative real-time PCR was used to detect differences in SOD2-gene expression after 6 hours and apoptotic activity was detected after 6 hours using propidium iodide flow cytometry. - RESULTS: Recipient preconditioning improved reperfusion damage index from 12.8±1.6 in controls to 8.8±1.8 (p<0.001). Serum levels of creatinine and BUN decreased from 4.29±0.25 mg/dl and 119±23 mg/dl in controls to 3.65±0.7 mg/dl and 81±19 mg/dl (p<0.05). The number of severely injured tubules decreased (p<0.05). Apoptotic activity was increased in SFN-treated rats. Mitochondrial microstructure was better preserved after SFN, while SOD 2 gene expression increased (p<0.05). - CONCLUSIONS: SFN ameliorates ischemia/reperfusion injury after KTx, most likely through anti-oxidative effects.