Komatsu H, Yaju H, Chiba K, Okumoto T
Research Laboratories, Yoshitomi Pharmaceutical Industries, Ltd, Saitama, Japan.
Int J Immunopharmacol. 1991;13(8):1137-46. doi: 10.1016/0192-0561(91)90165-4.
The effects of cyclo-oxygenase inhibitors on interleukin-6 (IL-6) production by human peripheral blood mononuclear cells were examined. Indomethacin and Y-9223, a novel cyclo-oxygenase inhibitor, inhibited the increases in the IL-6 level in the culture medium of both mitogen-stimulated adherent cells and non-adherent cells fractionated from mononuclear cells. Northern blotting showed that the mitogen-induced increase in the expression of IL-6 mRNA was inhibited by indomethacin and Y-9223, indicating that these agents inhibit IL-6 biosynthesis. Aspirin, ibuprofen, and phenylbutazone also inhibited IL-6 production by adherent cells stimulated with lipopolysaccharide (LPS). There was, however, no direct relationship between inhibition of IL-6 and prostaglandin E2 (PGE2) production by these agents. The addition of PGE2 corresponding to the amount produced by adherent cells stimulated with LPS slightly increased IL-6 production by unstimulated adherent cells, but to a lower level than that reached with LPS. An anti-PGE2 antibody partially blocked IL-6 production by adherent cells stimulated with LPS. These results suggest that, in addition to the inhibition of PGE2 production, other mediators including cyclooxygenase products or other action mechanisms are involved in the inhibition of IL-6 production by these drugs.
研究了环氧化酶抑制剂对人外周血单个核细胞产生白细胞介素-6(IL-6)的影响。吲哚美辛和新型环氧化酶抑制剂Y-9223抑制了从单个核细胞分离出的有丝分裂原刺激的贴壁细胞和非贴壁细胞培养基中IL-6水平的升高。Northern印迹显示,吲哚美辛和Y-9223抑制了有丝分裂原诱导的IL-6 mRNA表达增加,表明这些药物抑制IL-6生物合成。阿司匹林、布洛芬和保泰松也抑制脂多糖(LPS)刺激的贴壁细胞产生IL-6。然而,这些药物对IL-6的抑制与前列腺素E2(PGE2)的产生之间没有直接关系。添加与LPS刺激的贴壁细胞产生的量相当的PGE2,可使未刺激的贴壁细胞的IL-6产生略有增加,但低于LPS刺激达到的水平。抗PGE2抗体部分阻断LPS刺激的贴壁细胞产生IL-6。这些结果表明,除了抑制PGE2产生外,包括环氧化酶产物或其他作用机制在内的其他介质也参与了这些药物对IL-6产生的抑制作用。