Rieder H, Ramadori G, Meyer zum Büschenfelde K H
I. Medizinische Klinik, Johannes Gutenberg-Universität, Mainz, F.R.G.
J Hepatol. 1988 Dec;7(3):345-51. doi: 10.1016/s0168-8278(88)80007-2.
In the preceding paper it was shown that Kupffer cells isolated by digestion of the liver and purified by centrifugal elutriation can be activated in vitro by lipopolysaccharide and muramyl dipeptide to an enhanced superoxide response upon zymosan phagocytosis. Lipopolysaccharide and muramyl dipeptide also led to a strongly increased prostaglandin E2 release during the phagocytosis of zymosan. This activation was accompanied by an increased production of prostaglandin E2 during the incubation with the stimuli. Prostaglandin E2 synthesis was inhibited by the cyclooxygenase inhibitor indomethacin, reduced by dexamethasone, but only slightly decreased by the lipoxygenase inhibitor nordihydroguaiaretic acid. Indomethacin and dexamethasone also reduced the superoxide response, which only in the case of indomethacin is reversed by exogenous prostaglandin E2. Dexamethasone reduced the superoxide response in unstimulated cells as well. From these results it is deduced that cyclo-oxygenase products, especially prostaglandin E2, but not lipoxygenase products, i.e. leukotrienes, play some regulatory role in the activation process of Kupffer cells; in addition, a prostaglandin-independent inhibition exerted by dexamethasone seems to exist.
在前一篇论文中已表明，通过肝脏消化分离并用离心淘析法纯化的库普弗细胞，在体外可被脂多糖和胞壁酰二肽激活，从而在吞噬酵母聚糖时增强超氧化物反应。脂多糖和胞壁酰二肽在酵母聚糖吞噬过程中还导致前列腺素E2释放大幅增加。这种激活伴随着在与刺激物孵育期间前列腺素E2产量的增加。前列腺素E2的合成被环氧化酶抑制剂吲哚美辛抑制，被地塞米松降低，但仅被脂氧合酶抑制剂去甲二氢愈创木酸轻微降低。吲哚美辛和地塞米松也降低了超氧化物反应，仅在吲哚美辛的情况下，外源性前列腺素E2可使其逆转。地塞米松也降低了未受刺激细胞的超氧化物反应。从这些结果可以推断，环氧化酶产物，尤其是前列腺素E2，而非脂氧合酶产物，即白三烯，在库普弗细胞的激活过程中发挥一些调节作用；此外，似乎存在地塞米松施加的不依赖前列腺素的抑制作用。
