- 作者: 趙祖怡; 丁慶雄; 朱燦銘; 葉明陽
- 作者服務機構: 國防醫學院內科學科暨三軍總醫院血液腫瘤科; 國防醫學院微生物及免疫學科; 美國紐約州羅斯威爾派克學院診斷免疫及生化系
- 中文摘要: 在本研究中我們檢測了三種非固醇類抗炎藥物對人類淋巴素活化殺手細胞活性生成之影響,淋巴素活化殺手細胞活性的生成是將由正常人週邊血液分離出之單核細胞與合成介白質2共同培養3至4天而得。其活性之檢測是藉4小時鉻-51釋放試驗完成,以K-562及HL-60細胞株作為標的細胞。我們發現三種藥物在濃度為5×10M下僅有in-domethacin對淋巴素活化殺手細胞活性之生成具有增強效應。此外,我們也對這三種藥物對培養液中前列腺素E2之生成作了檢測;結果顯示這三種藥物均能有效地抑制培養液中前列腺素E2之生成。Indomethacin在體外實驗中增強人類淋巴素活化殺手細胞活性之生成之機轉可能並不僅止於前列腺素E2生成之抑制。
- 英文摘要: The effects of three nonsteroidal antiinflammatory drugs (NSAIDs),namely, indomethacin, aspirin,and mefenamate (ponstan), on the lymphokine-activated killer (LAK) cell activities generated from co-culturing recombinant interleukin-2 (rIL-2) and normal human peripheral blood mononuclear cells (PBMCs)for 3 to 4 days were investigated. The LAK cell activities were measured by a 4 hour Cr release micro-cytotoxicity assay using HL-60 and K-562 as target cells. Indomethacin was found to have significantaugmenting effect on LAK cell activity at the concentration of 5 X 10M, whereas aspirin and ponstandid not show the same effect at the same concentration. Additional experiments, however, demonstratedthat all of these 3 agents could effectively suppress the production of prostaglandin E2 (PGE2) in theculture medium. These results indicated that PGE2 suppression may not be the only mechanism of in-domethacin for upregulation of LAK cell activity, and even immune functions.
- 中文關鍵字: NSAIDs; LAK cell activity
- 英文關鍵字: --