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应用离体细胞体外孵育法研究了反义ｃｍｙｃ寡脱氧核苷酸（反义ｃｍｙｃＯＤＮ）对大鼠黄体细胞人绒毛膜促性腺激素（ｈＣＧ）诱导的孕酮（Ｐ）和雌二醇（Ｅ２）生成的影响及其与外源性ｃＡＭＰ和Ｃａ２＋的关系。结果发现，反义ｃｍｙｃＯＤＮ能呈剂量相关方式抑制黄体细胞ｈＣＧ诱导的Ｐ和Ｅ２的生成。在浓度分别为１０和５μｍｏｌ／Ｌ时的抑制作用即具有显著意义（Ｐ＜０．０５）；而无义ｔａｔ寡脱氧核苷酸则无此作用。反义ｃｍｙｃＯＤＮ对黄体细胞ｈＣＧ诱导的Ｐ和Ｅ２产生的抑制作用能被加入１０－４ｍｏｌ／Ｌ二丁酰ｃＡＭＰ逆转，钙离子通道阻断剂维拉帕米对此种抑制作用具有协同效应。结果提示，ｃｍｙｃ癌基因参与黄体细胞ｈＣＧ诱导的Ｐ和Ｅ２生成的调控。
In vitro incubation of cells in vitro study antisense c myc oligodeoxynucleotides (antisense c mycODN) on rat luteal cells human chorionic gonadotropin (hCG) -induced progesterone (P) and estrogen The Effect of Alcohol (E2) Production and Its Relationship with Exogenous cAMP and Ca2 +. The results showed that antisense c mycODN can dose-dependent manner inhibited luteal cells hCG induced P and E2 generation. The inhibitory effect was significant at concentrations of 10 and 5 μmol / L, respectively (P <0.05), while non-sense oligodeoxynucleotides did not. Anti-sense c mycODN on luteal cells hCG-induced P and E2 production can be inhibited by adding 10-4mol / L dibutyryl cAMP reverse calcium channel blocker verapamil has a synergistic effect on this inhibition . The results suggest that c myc oncogene involved in luteal cells hCG-induced P and E2 generation regulation.