Induction of specific stress response increases resistance of rat liver allografts to cold ischemia and reperfusion injury

Induction of specific stress response increases resistance of rat liver allografts to cold ischemia and reperfusion injury

Heme oxygenase-1 (HO-1) has been shown to increase cellular resistance against oxidative injury, but the functional significance of this is currently obscure. We investigated the protective role of HO-1, induced by tin-protoporphyrin IX (SnPP), in attenuating liver transplantation injury. Lewis rats...

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Veröffentlicht in:Transplant international 2003-06, Vol.16 (6), p.396
Hauptverfasser: Uchida, Yasushi, Tamaki, Tohru, Tanaka, Mitsuko, Kaizu, Takashi, Sei-ichiro Tsuchihashi, Takahashi, Tsuyoshi, Kawamura, Akio, Kakita, Akira
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container_issue 6
container_start_page 396
container_title Transplant international
container_volume 16
creator Uchida, Yasushi
Tamaki, Tohru
Tanaka, Mitsuko
Kaizu, Takashi
Sei-ichiro Tsuchihashi
Takahashi, Tsuyoshi
Kawamura, Akio
Kakita, Akira
description Heme oxygenase-1 (HO-1) has been shown to increase cellular resistance against oxidative injury, but the functional significance of this is currently obscure. We investigated the protective role of HO-1, induced by tin-protoporphyrin IX (SnPP), in attenuating liver transplantation injury. Lewis rats were intraperitoneally treated with saline as control, 50 µmol/kg of SnPP, or 2 mg/kg of cycloheximide (CHX) before SnPP injection. Gene expression of HO-1 was induced after either treatment with SnPP- or CHX + SnPP instead of saline, whereas HO-1 protein synthesis was enhanced in Kupffer-like dendritic cells of the SnPP-treated group. Following reperfusion of liver grafts preserved for 30 h, there were fewer intercellular adhesion molecule-1-positive cells in SnPP-treated livers, significantly reduced numbers of dead cells, and enhanced graft viability. The present data suggest that increased synthesis of HO-1 protein by SnPP pre-conditioning is linked to the improved liver graft viability through inhibition of inflammatory adhesion molecules.
doi_str_mv 10.1007/s00147-003-0550-1
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title Induction of specific stress response increases resistance of rat liver allografts to cold ischemia and reperfusion injury
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