重组肿瘤坏死因子和白细胞介素-1均能刺激人滑膜细胞花生四烯酸释放及磷脂代谢。

Recombinant tumor necrosis factor and interleukin-1 both stimulate human synovial cell arachidonic acid release and phospholipid metabolism.

作者信息

Godfrey R W, Johnson W J, Hoffstein S T

出版信息

Biochem Biophys Res Commun. 1987 Jan 15;142(1):235-41. doi: 10.1016/0006-291x(87)90476-1.

Abstract

Stimulation of [3H]-arachidonic acid labeled human synovial cells with 3.0 X 10(-10)M recombinant interleukin-1 or tumor necrosis factor resulted in the release of incorporated radiolabel (41.1% and 27.7% respectively). Analysis of [3H]-arachidonic acid labeled phospholipids showed that interleukin-1 and tumor necrosis factor diminished [3H]-arachidonic acid in phosphatidyl-choline phosphatidylserine and phosphatidylinositol. Treatment of [3H]-arachidonic acid labeled cells with 10(-3)M dibutyryl cyclic AMP or 10(-6)M PGE2 did not affect spontaneous or stimulated [3H] arachidonic acid release significantly. These data show that recombinant interleukin-1 and tumor necrosis factor stimulate human synovial cell phospholipase activity in a similar manner and that this activity is not affected significantly by agents that elevate cyclic AMP.

摘要

用3.0×10⁻¹⁰M重组白细胞介素 -1或肿瘤坏死因子刺激[³H] - 花生四烯酸标记的人滑膜细胞，导致掺入的放射性标记物释放（分别为41.1%和27.7%）。对[³H] - 花生四烯酸标记的磷脂分析表明，白细胞介素 -1和肿瘤坏死因子减少了磷脂酰胆碱、磷脂酰丝氨酸和磷脂酰肌醇中的[³H] - 花生四烯酸。用10⁻³M二丁酰环磷酸腺苷或10⁻⁶M前列腺素E2处理[³H] - 花生四烯酸标记的细胞，对自发或刺激的[³H]花生四烯酸释放没有显著影响。这些数据表明，重组白细胞介素 -1和肿瘤坏死因子以类似方式刺激人滑膜细胞磷脂酶活性，且该活性不受升高环磷酸腺苷的试剂的显著影响。