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硫代乙醇酸盐诱导的大鼠腹腔巨噬细胞中,磷脂质量增加而花生四烯酰分子种类减少,这与类花生酸合成减少及肿瘤坏死因子合成增加有关。

Increased phospholipid mass with decreased arachidonoyl molecular species is associated with decreased eicosanoid synthesis and increased tumor necrosis factor synthesis by thioglycollate-elicited rat peritoneal macrophages.

作者信息

Carrick J B, Moore J N, Chapkin R S, Schnellmann R G

机构信息

Department of Large Animal Medicine and Physiology, College of Veterinary Medicine, University of Georgia, Athens 30602, USA.

出版信息

Shock. 1995 Apr;3(4):284-91.

PMID:7600195
Abstract

Because the activation state of macrophages may alter their response to endotoxin, we compared phospholipid arachidonic acid content, and synthesis of eicosanoids and tumor necrosis factor by resident and thioglycollate-elicited rat peritoneal macrophages. Thioglycollate elicitation increased macrophage phospholipid mass twofold, increased the relative percentages of 16:0-20:4 diacylglycerophosphocholine (PtdCho) and 18:0-20:4 diacylglycerophosphoethanolamine (PtdEtn), and decreased the relative percentages of 18:0-20:4 alkenylacylglycerophosphoethanolamine (PlsEtn) and 18:0-20:4 alkylacylglycerophosphocholine (PakCho) compared with resident peritoneal macrophages. Thioglycollate-elicited macrophages synthesized significantly less thromboxane B2, 6-keto-prostaglandin F1 alpha, and prostaglandin E2 and more tumor necrosis factor (TNF) activity in response to both endotoxin and A23187 than did resident macrophages. These results suggest that thioglycollate elicitation decreases specific arachidonic acid-containing molecular species in PlsEtn and PakCho, which may, in part, explain the decrease in eicosanoid and increase in TNF synthesis by thioglycollate-elicited macrophages. The differences between resident and thioglycollate-elicited macrophages in the synthesis of the eicosanoids and TNF activity was not altered by increasing either the concentration of either stimulus or the incubation time.

摘要

由于巨噬细胞的激活状态可能会改变其对内毒素的反应,我们比较了正常大鼠和经巯基乙酸诱导的大鼠腹腔巨噬细胞的磷脂花生四烯酸含量、类花生酸和肿瘤坏死因子的合成。与正常腹腔巨噬细胞相比,巯基乙酸诱导使巨噬细胞磷脂质量增加了两倍,16:0 - 20:4二酰基甘油磷酸胆碱(PtdCho)和18:0 - 20:4二酰基甘油磷酸乙醇胺(PtdEtn)的相对百分比增加,而18:0 - 20:4烯基酰基甘油磷酸乙醇胺(PlsEtn)和18:0 - 20:4烷基酰基甘油磷酸胆碱(PakCho)的相对百分比降低。在对内毒素和A23187的反应中,巯基乙酸诱导的巨噬细胞合成的血栓素B2、6 - 酮 - 前列腺素F1α和前列腺素E2明显减少,而肿瘤坏死因子(TNF)活性则比正常巨噬细胞更高。这些结果表明,巯基乙酸诱导降低了PlsEtn和PakCho中特定含花生四烯酸的分子种类,这可能部分解释了巯基乙酸诱导的巨噬细胞类花生酸合成减少和TNF合成增加的现象。正常巨噬细胞和巯基乙酸诱导的巨噬细胞在类花生酸合成和TNF活性方面的差异,不会因增加刺激物浓度或孵育时间而改变。

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引用本文的文献

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Mol Cell Biochem. 1996 Dec 20;165(2):135-43. doi: 10.1007/BF00229475.