摘要
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。
It has been shown in the present study that transmembrane tumor necrosis factor (TMTNFα)and secretory TNFα(S-TNFα) could induce a large amounts of PGE_2 release from target cell lines (P<0. 01),as they were exerting their cytotoxic activity. Indomethacin, an inhibitor of cyclooxygenase (COX),was able not only to block partially or most TM-TNFα induced PGE_2 synthesis in the target cells (P<0. 01), but also to inhibit its cytocidal effect. The trend of inhibitory effect on the PGE_2 release induced by TM-TNFα was consistent with that on the cytotoxicity of TM-TNFα. In contrast to TM-TNFα, these effects of S-TNFα remained unchanged, whether indomethacin was present or not. These results suggested that PGE_2 may be involved in the signal transduction pathway of both forms of TNF-α to cause target cell death, but the action levels of both in enhancing PGE_2 synthesis may be different.
出处
《同济医科大学学报》
CSCD
2000年第1期14-16,共3页
Acta Universitatis Medicinae Tongji
基金
国家自然科学基金!(No.39570796)
关键词
肿瘤坏死因子
跨膜型
分泌型
前列腺素E
tumor necrosis factor
transmembrane
secretory
cytotoxicity
prostaglandins E
