COMPLEMENT ACTIVATES KUPFFER CELLS AND NEUTROPHILS DURING REPERFUSION AFTER HEPATIC ISCHEMIA
COMPLEMENT ACTIVATES KUPFFER CELLS AND NEUTROPHILS DURING REPERFUSION AFTER HEPATIC ISCHEMIA
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DOI：
10.1152/ajpgi.1993.264.4.g801
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发表时间：
1993-04-01
影响因子：
--
通讯作者：
SPITZER, JJ
中科院分区：
文献类型：
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作者：
JAESCHKE, H;FARHOOD, A;SPITZER, JJ
在雄性Fischer大鼠肝缺血（45 min）和再灌注模型中研究补体因子可能参与枯否细胞（KC）和多形核中性粒细胞（PMN）的缺血后激活的假说。缺血前血清补体的耗尽导致KC诱导的氧化应激显着减弱（血浆谷胱甘肽的氧化增强），并且还防止了在1小时的初始再灌注期间肝脏中中性粒细胞的积聚。通过注射眼镜蛇毒因子（CVF; 75 μ g CVF/kg）的补体激活也诱导了血浆谷胱甘肽的氧化增强和肝脏中中性粒细胞的积累。CVF处理后1小时，从肝脏分离KC和PMN，证明了与在缺血后肝脏中观察到的佛波醇肉豆蔻酸酯乙酸酯和调理剂酵母聚糖刺激类似的引发效应。补体耗尽的动物和动物预处理的可溶性人补体受体1型（BRL 55730; 22.5毫克/公斤）积累了显着较少的中性粒细胞在缺血后的肝脏在较长的再灌注期（24小时），并持续显着减少损伤。它的结论是，补体参与诱导KC诱导的氧化应激，启动KC和中性粒细胞增强活性氧的产生，并在再灌注过程中的肝脏中的中性粒细胞的不断积累。
The hypothesis that complement factors may be involved in the postischemic activation of Kupffer cells (KC) and polymorphonuclear neutrophils (PMN) was investigated in a model of hepatic ischemia (45 min) and reperfusion in male Fischer rats in vivo. Depletion of serum complement before ischemia resulted in a significant attenuation of the KC-induced oxidant stress (enhanced oxidation of plasma glutathione) and also prevented the accumulation of PMNs in the liver during the initial reperfusion period of 1 h. Complement activation through injection of cobra venom factor (CVF; 75 mug CVF/kg) also induced enhanced oxidation of plasma glutathione and accumulation of PMNs in the liver. Isolation of KC and PMNs from the liver 1 h after CVF treatment demonstrated a similar priming effect for stimulation with phorbol myristate acetate and opsonized zymosan as was observed in the postischemic liver. Complement-depleted animals and animals pretreated with the soluble human complement receptor type 1 (BRL 55730; 22.5 mg/kg) accumulated significantly less PMNs in the postischemic livers during longer reperfusion periods (24 h) and sustained significantly less injury. It is concluded that complement is involved in the induction of a KC-induced oxidant stress, the priming of KC and PMNs for enhanced reactive oxygen generation, and the continuous accumulation of PMNs in the liver during reperfusion.