Vollmar B, Wanner G A, Stöckle V, Bauer M, Menger M D
Institut für Klinisch-Experimentelle Chirurgie, Universität des Saarlandes, Homburg/Saar.
Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):403-4.
In endotoxin-exposed rat livers, G-CSF caused a reduction of CINC gene transcripts in the nonparenchymal cell fraction, which might be the mechanism for attenuation of microvascular leukocyte adherence and leukocyte-dependent tissue injury, as observed upon G-CSF application in a model of endotoxin-induced hepatotoxicity.
在内毒素暴露的大鼠肝脏中,粒细胞集落刺激因子(G-CSF)导致非实质细胞部分中细胞因子诱导的中性粒细胞趋化因子(CINC)基因转录物减少,这可能是微血管白细胞黏附和白细胞依赖性组织损伤减轻的机制,如在内毒素诱导的肝毒性模型中应用G-CSF时所观察到的那样。