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目的：观察吗丙嗪（Ｐｒｏ）和阿霉素（Ｄｏｘ）合用对肿瘤细胞周期及ＤＮＡ合成的影响，以探讨吗丙嗪增强阿霉素抗肿瘤作用之机制。方法：采用拒染法观察Ｐｒｏ，Ｄｏｘ和Ｐｒｏ＋Ｄｏｘ对小鼠体外艾氏腹水癌细胞（ＥＡＣ）的杀伤作用；采用标记前体物参入法和显微分光光度术观察两药合用对ＥＡＣ细胞周期及ＤＮＡ合成的影响。结果：Ｐｒｏ２１．４６，４２．９２和６４．３８μｍｏｌ·Ｌ－１增强Ｄｏｘ对ＥＡＣ细胞的杀伤作用；Ｐｒｏ（２１４．５９μｍｏｌ·Ｌ－１）和Ｄｏｘ（１８．０２μｍｏｌ·Ｌ－１）合用对ＥＡＣ细胞ＤＮＡ合成有明显的抑制作用；用药后４～８ｈＧ１期细胞增加，ＤＮＡ直方图左移，各用药组细胞分裂指数无明显差异。结论：Ｐｒｏ可增强Ｄｏｘ的抗肿瘤作用，其机理可能与Ｐｒｏ加强Ｄｏｘ对ＤＮＡ合成的抑制及对Ｇ１期细胞累积作用增强有关。
OBJECTIVE: To observe the effects of combination of promazine (Pro) and doxorubicin (Dox) on the cell cycle and DNA synthesis of tumor cells, and to explore the mechanism of the anti-tumor effect of mpromazine on doxorubicin. Methods: Anti-Eca antibody was used to observe the killing effect of Pro, Dox and Pro + Dox on mouse Echocardiocytoma cells (EAC) in vitro. The precursor incorporation and microspectrophotometry were used to observe the effects of two drugs on cell cycle, Effects of DNA synthesis. Results: Pro21.46,42.92 and 64.38μmol·L-1 enhanced the killing effect of Dox on EAC cells. Pro (214.59μmol·L-1) and Dox (18.02μmol·L-1) Cell DNA synthesis significantly inhibited; 4 ~ 8hG1 after treatment cells increased DNA histogram shift to the left, each drug group cell division index no significant difference. Conclusion: Pro can enhance the antitumor effect of Dox. The mechanism may be related to the inhibition of DNA synthesis by Pro and Dox on Progenitor cell proliferation in G1 phase.