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目的：以Ｄｅｘ诱导小鼠胸腺细胞凋亡为模型，研究细胞因子（ＩＬ２、ＩＬ６）对小鼠胸腺细胞凋亡的调节作用。方法：应用ＰＩ法检测亚二倍体细胞，二苯胺法测定胸腺细胞片段化ＤＮＡ含量（％），ＤＮＡ凝胶电泳，流式细胞计分析胸腺细胞表型、测定高钙细胞百分比。结果：发现地塞米松（Ｄｅｘ）与小鼠胸腺细胞共同培养引起细胞凋亡，胸腺细胞减少以ＣＤ４＋ＣＤ８＋细胞最明显。细胞凋亡具有时间效应并与Ｄｅｘ浓度有关。３～４ｗ小鼠胸腺细胞对Ｄｅｘ的敏感性高于６～８ｗ小鼠。高浓度（＞２００Ｕ／ｍｌ）ＩＬ２或１００Ｕ／ｍｌＩＬ２与ＩＬ６（１００Ｕ／ｍｌ）协同可减轻Ｄｅｘ诱导的胸腺细胞凋亡，其片段化ＤＮＡ和亚二倍体细胞明显减少，胞浆Ｃａ２＋浓度降低，胸腺细胞亚群分布得到纠正。单独应用ＩＬ６不能改变Ｄｅｘ诱导的胸腺细胞凋亡。结论：地塞米松可促进小鼠胸腺细胞凋亡，高浓度（＞２００Ｕ／ｍｌ）ＩＬ２或１００Ｕ／ｍｌＩＬ２与ＩＬ６（１００Ｕ／ｍｌ）协同可减轻Ｄｅｘ诱导的胸腺细胞凋亡。
Objective: Dex induced thymocyte apoptosis in mice as a model to study the cytokines (IL 2, IL 6) on the regulation of thymocyte apoptosis in mice. Methods: The sub-diploid cells were detected by PI method. The DNA content (%) of thymocytes was determined by diphenylamine method. The thymocyte phenotypes were analyzed by flow cytometry. The percentage of high calcium cells was determined. Results: It was found that dexamethasone (Dex) co-cultured with mouse thymus cells caused apoptosis, and the reduction of thymus cells was the most obvious in CD4 + CD8 + cells. Apoptosis has a time effect and is related to Dex concentration. 3 ~ 4w mouse thymocytes sensitivity to Dex than 6 ~ 8w mice. High concentration (> 200U / ml) IL 2 or 100U / ml IL 2 and IL 6 (100U / ml) Synergy can reduce Dex induced thymocyte apoptosis, the fragment of DNA and sub-diploid cells was significantly reduced, Cytoplasmic Ca2 + concentration decreased, thymus cell subpopulation was corrected. IL 6 alone can not change Dex-induced thymocyte apoptosis. Conclusion: Dexamethasone can promote the apoptosis of thymocytes in mice. Dex-induced thymocyte apoptosis can be alleviated by synergistic treatment with high concentration (> 200U / ml) IL-2 or 100U / ml IL-2 and IL-6 .