Taurine Protects from Liver Injury after Warm Ischemia in Rats: The Role of Kupffer Cells

Background/Aims: Warm ischemia to liver with subsequent Kupffer cell-dependent pathology is associated with many clinical conditions. Taurine prevents Kupffer cell activation and improves graft survival after experimental cold ischemia and liver transplantation. Thus this study was designed to asses...

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Veröffentlicht in:European surgical research 2007-01, Vol.39 (5), p.275-283
Hauptverfasser: Kincius, M., Liang, R., Nickkholgh, A., Hoffmann, K., Flechtenmacher, C., Ryschich, E., Gutt, C.N., Gebhard, M.-M., Schmidt, J., Büchler, M.W., Schemmer, P.
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Sprache:eng
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Zusammenfassung:Background/Aims: Warm ischemia to liver with subsequent Kupffer cell-dependent pathology is associated with many clinical conditions. Taurine prevents Kupffer cell activation and improves graft survival after experimental cold ischemia and liver transplantation. Thus this study was designed to assess its effects after warm hepatic ischemia. Methods: The left liver lobe of female Sprague-Dawley rats (170–210 g) underwent 60 min of warm ischemia. Animals were given either intravenous taurine or Ringer’s solution 10 min prior to warm ischemia. Transaminases, histology, in vivo microscopy, intercellular adhesion molecules-1 (ICAM-1) expression, TNF-α and tissue hydroperoxide were compared between groups using analysis of variance (ANOVA) or ANOVA on ranks as appropriate. Results: Taurine significantly decreased transaminases and improved histologic outcome. Phagocytosis of latex beads, serum TNF-α levels and tissue hydroperoxide concentrations were also significantly reduced. Stickers in sinusoids and post-sinusoidal venules significantly decreased. In parallel, both leukocyte infiltration and ICAM-1 expression decreased (p < 0.05), while flow velocity of red blood cells as well as sinusoidal perfusion rate were improved (p < 0.05). Conclusion: This study demonstrates that taurine blunts Kupffer cell-dependent hepatic pathology after warm ischemia in vivo via mechanisms including leukocyte-endothelial interaction, microcirculation disturbances and protection against lipid peroxidation.
ISSN:0014-312X
1421-9921
DOI:10.1159/000102982