摘要目的:通过观察雷公藤内酯醇诱导BALB/c小鼠脾细胞凋亡与细胞活化程度的关系，探讨该化合物免疫抑制的作用机理。方法:以脾淋巴细胞为研究对象，PHA-P、PMA和rhIL-2为有丝分裂原活化淋巴细胞。结合荧光染色法，DNA凝胶电泳及DNA片段测定等方法，检测雷公藤内酯醇诱导凋亡的作用。结果:（1）雷公藤内酯醇能够造成活化的淋巴细胞凋亡，并呈浓度依赖性；（2）雷公藤内酯醇不能使处于静止状态的脾淋巴细胞凋亡；（3）雷公藤内酯醇诱导淋巴细胞凋亡的作用，与淋巴细胞的活化程度和增殖反应程度密切。结论:雷公藤内酯醇不能造成静止状态的淋巴细胞发生细胞凋亡，只能够诱导已活化淋巴细胞发生细胞凋亡，并以此影响机体的免疫功能。

abstractsObjective:To study the mechanisms of Triptolide on immunosuppression by means of observation on Triptolide-induced apoptosis of activated lymphocytes. Methods:Spleen cells of BALB/c mice were stimulated by mitogen such as PHA-P, PMA and interleukin-2 (rhIL-2). Activity and apoptosis of lymphocytes were measured with 3H-TdR incorporation, and with DNA fragment determination and membrane damage, respectively. Results:Triptolide could induce apoptosis of activated lymphocytes in dose-dependent fashion, but not resting lymphocytes. The degree of susceptibility to apoptosis was correlated with the levels of cell cycling as measured by 3H-TdR incorporation during S phase; and DNA fragmentation was associated proportionally with time elapse after adding Triptolide. The number of cells in S phase was proportional to the amount of apoptotic cells induced by Triptolide.Conclusion:These data suggest that the suicide of activated cycling T cells induced by Triptolide may be one of the mechanisms for the immunosuppression.