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目的：探讨肿瘤细胞受照后 Ｇ２／ Ｍ 期阻滞和凋亡的关系及调控。方法：以 Ｋ５６２ 细胞为对象，用流式细胞仪、形态学、 Ｄ Ｎ Ａ 电泳和凋亡蛋白２ ．７（ Ａ Ｐ Ｏ２．７） 等方法检测细胞周期和凋亡。结果：（１）２０ Ｇｙ γ射线照射 Ｋ５６２细胞后引起 Ｇ２／ Ｍ 期阻滞， ４８ ｈ Ｇ２／ Ｍ 期比例为７１ ．２ ％ ， 流式细胞仪、形态学和 Ａ Ｐ Ｏ２ ．７ 检测凋亡比例分别为２．６％ 、２ ．０ ％ ±１ ．１ ％ 和２２ ．５ ％ ；（２） 照前加入１０ ｍ ｍｏｌ／ Ｌ 咖啡因， Ｇ２／ Ｍ 比例降低至１２ ．０ ％ ，凋亡比例增至１３．５％ 、２０．１％ ±３ ．５ ％ 和３４．４％ ，明显高于单纯照射组（ Ｐ＜ ０ ．０１） 。咖啡因本身对细胞周期和凋亡没有影响。结论：抑制 Ｇ２／ Ｍ 期阻滞可促进辐射诱导的凋亡，为提高肿瘤细胞的辐射敏感性提供一个新思路。
Objective: To investigate the relationship between G2/M arrest and apoptosis after tumor cells exposure and its regulation. Methods: K562 cells were used as flow cytometry, morphology, D N A electrophoresis and apoptosis protein 2 . 7 (A P O2.7) and other methods to detect cell cycle and apoptosis. Results: (1) G2/M phase arrest was induced by irradiation of K562 cells with 20 Gy γ-rays, and the ratio of G2/M phase at 48 h was 71. 2%, flow cytometry, morphology and A P O2. 7 The proportion of apoptosis detected was 2.6% and 2. 0 % ±1 . 1 % and 22 . 5%; (2) Add 10 m mol/L caffeine as before, G2/M ratio is reduced to 12. At 0%, the proportion of apoptosis increased to 13.5% and 20.1% ±3. 5% and 34.4% were significantly higher than those in the simple irradiation group (P < 0.01). Caffeine itself has no effect on cell cycle and apoptosis. CONCLUSION: Inhibition of G2/M arrest can promote radiation-induced apoptosis and provide a new idea for improving the radiosensitivity of tumor cells.