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Differences in the involvement of prostanoids from Kupffer cells in the mediation of anaphylatoxin C5a-, zymosan-, and lipopolysaccharide-dependent hepatic glucose output and flow reduction.
Laboratory Investigation ( IF 5 ) Pub Date : 2003-12-01 , DOI: 10.1097/01.lab.0000101727.89483.37
Sabine Pestel 1 , Gerald Schlaf , Otto Götze , Kurt Jungermann , Henrike L Schieferdecker
Affiliation  

Various inflammatory stimuli such as anaphylatoxin C5a, zymosan, and lipopolysaccharides (LPSs) have been reported both to enhance glucose output in the perfused rat liver and to induce prostanoid (ie, prostaglandin and thromboxane) release from Kupffer cells, the resident liver macrophages. Because prostanoids can enhance glucose output from hepatocytes, it was the aim of this study to compare the possible roles of prostanoids released after C5a, zymosan, and LPS in the mediation of hepatic glucose output. In perfused livers both C5a and zymosan immediately enhanced glucose output, reduced flow, and induced prostanoid overflow into the hepatic vein, but with different quantities and kinetics. Only the C5a-induced but not the zymosan-induced effects were abrogated by inhibitors of prostanoid signaling as the prostanoid synthesis inhibitor indomethacin and the thromboxane receptor antagonist daltroban. In contrast to C5a and zymosan, LPS had no effect on glucose output, flow rate, or prostanoid overflow. In isolated Kupffer cells, C5a and zymosan induced maximal release of prostaglandins D(2) and E(2) and of thromboxane A(2) within a period of 0 to 2 minutes and 5 to 15 minutes, respectively. In pulse-chase experiments, maximal prostanoid release was already observed after 2 minutes of continuous stimulation with C5a, but only after 10 to 15 minutes of continuous stimulation with zymosan. LPS-dependent prostanoid release was not seen before 1 hour. Thus, even though C5a, zymosan, and LPS induced prostanoid release from Kupffer cells, only C5a quickly regulated hepatic glucose metabolism in a prostanoid-dependent manner (due to the kinetics and quantities of prostanoids released).

中文翻译:

来自 Kupffer 细胞的前列腺素参与介导过敏毒素 C5a、酵母聚糖和脂多糖依赖性肝葡萄糖输出和流量减少的差异。

据报道,各种炎症刺激物(例如过敏毒素 C5a、酵母聚糖和脂多糖 (LPS))既可以增强灌注大鼠肝脏中的葡萄糖输出,又可以诱导枯否细胞(常驻肝巨噬细胞)释放前列腺素(即前列腺素和血栓素)。因为前列腺素可以增强肝细胞的葡萄糖输出,本研究的目的是比较 C5a、酵母聚糖和 LPS 后释放的前列腺素在介导肝葡萄糖输出中的可能作用。在灌注肝脏中,C5a 和酵母聚糖立即增加葡萄糖输出,减少流量,并诱导前列腺素溢出到肝静脉,但数量和动力学不同。只有 C5a 诱导而非酵母聚糖诱导的作用被前列腺素信号转导抑制剂如前列腺素合成抑制剂吲哚美辛和血栓素受体拮抗剂达曲班消除。与 C5a 和酵母聚糖相比,LPS 对葡萄糖输出、流速或前列腺素溢出没有影响。在孤立的 Kupffer 细胞中,C5a 和酵母聚糖分别在 0 到 2 分钟和 5 到 15 分钟的时间内诱导前列腺素 D(2) 和 E(2) 以及血栓素 A(2) 的最大释放。在脉冲追踪实验中,在用 C5a 连续刺激 2 分钟后,已经观察到最大的前列腺素释放,但仅在用酵母聚糖连续刺激 10 到 15 分钟后才观察到。1 小时前未见 LPS 依赖性前列腺素释放。因此,即使 C5a、酵母聚糖和 LPS 诱导枯否细胞释放前列腺素,
更新日期:2019-11-01
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