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研究比较前列腺素Ｅ_２（ＰＧＥ_２）对两型肿瘤坏死因子（ＴＮＦ－ａ）胞毒效应。结果：跨膜型ＴＮＦａ（ＴＭ－ＴＮＦａ）和分泌型ＴＮＦａ（Ｓ－ＴＮＦａ）在杀伤靶细胞的同时，可引起靶细胞释放大量ＰＧＥ_２（Ｐ＜０．０１）。用环氧化酶抑制剂消炎痛可部分或大部分阻断ＴＭ－ＴＮＦａ诱导靶细胞产生的ＰＧＥ_２（Ｐ＜０．０１），并且也可抑制ＴＭ－ＴＮＦａ的胞毒效应（Ｐ＜．０１），其抑制程度与 ＰＧＥ_２阻断程度一致。但消炎痛却不能阻断 Ｓ－ＴＮＦａ诱导其敏感靶细胞产生 ＰＧＥ_２，也不能抑制 Ｓ－ＴＮＦａ对其敏感靶细胞的杀伤作用。结果提示，ＰＧＥ_２可能参与二型ＴＮＦａ胞毒效应的信号传导，但是二型ＴＮＦａ引起靶细胞ＰＧＥ_２水平升高的作用环节可能存在差异。
To study the effects of prostaglandin E_2 (PGE_2) on the cytotoxicity of two types of tumor necrosis factor (TNF-α). Results: Both transmembrane TNFa (TM-TNFa) and secreted TNFa (S-TNFa) caused a large amount of PGE 2 release (P <0.01) while killing target cells. Indomethacin, an cyclooxygenase inhibitor, partially or mostly blocked PGE2 (P <0.01) induced by TM-TNFa in target cells and also inhibited the cytotoxic effect of TM-TNFa (P <.01) , The degree of inhibition is consistent with the extent of PGE 2 block. However, indomethacin can not block S-TNFa induced sensitive target cells to produce PGE_2, also can not inhibit the killing effect of S-TNFa on its sensitive target cells. The results suggest that PGE_2 might be involved in the signal transduction of cytotoxicity of type 2 TNFa. However, there may be differences in the role of type 2 TNFa in the elevation of PGE_2 in target cells.