择时电针干预荷乳腺癌C57BL／6J近交系小鼠对SCN钟基因正反馈环路表达的影响

目的：观察荷乳腺癌小鼠电针后其视交叉上核（SuprachiasmaticNucleus，SCN）中Bmall和ClockmRNA水平的变化，探讨电针对荷瘤动物自发性活动节律影响的正反馈环路的调控机制。方法：将C57BL／6J雄性小鼠随机分为空白组、模型组、模型加电针、空白加电针4组（每组6只）。针灸加模型组在造模成功后的第8-10d，于CT16相位（即：动物起始活动点后4h）进行电针治疗。所有的小鼠将在最后一次治疗后2h立即断颈处死，在相应部位取材后RT-PCR对指标进行检测。结果：检测结果显示，空白组的BmallmRNA，ClockmRNA表达要高于模型组，且模型加电针组的BmallmRNA，ClockmRNA表达要高于模型组。虽然上述结果无显著的统计学意义（P〉0．05），仍表现出一个改善的趋势。结论：本研究表明电针对荷乳腺癌小鼠在CTl6时相的治疗可升高SCNBmall以及ClockmRNA的表达使之趋于空白小鼠的表达，表明，电针干预可通过直接调控中枢Bmall以及Clock的表达，从而调节正反馈环路进而影响荷乳腺癌小鼠的自发性节律活动，对肿瘤的增殖有一定的抑制作用。

Improving Effects of Electroacupuncture on Regenerative Feedback Loop of Superchiasmatic Nucleus in Mice with Breast Cancer

Objective： To observe express changes of SCN （superehiasmatic nucleus） Bmall mRNA, Clock mRNA, in mice with breast cancer after eleereoaeunpuneture and to detect the regulatory mechanism of electroacupuneture effects on regenerative feed- back loop of superchiasmatic nucleusl in mice with breast cancer. Methods： C57BL/6J mice were randomly divided into 4 groups, healthy group （ n = 6）, model group （ n = 6）, model mice with electroacupuncture group （ n = 6） and healthy mice with electroacu- puncture （ n = 6） . Mice in treatment groups accepted acupuncture at CTI6 in the 82, 9th and 10th day after successfully modeling. All mice were sacrificed 2 hours later when accepted the third time treatment in order to extract samples and detect indexes with RT- PCR. Results： Bmall mRNA, Clock mRNA expressed in the model mice with electroacupuneture group increased when compared with model group; Clock mRNA in the healthy mice with electroacupuncture group also increased when compared with healthy group. These results demonstrated improving tendencies, even though all these results did not showed a statistical significance. Conclusions： This study show modulate effects of electroacupuncture on SCN Bmall mRNA, Clock mRNA express in C57BL/6J mice with breast cancer at CT16 thus to let it tend to normal level And the mechanism that electroacupuncture modulate the activity rhythm in mice with breastcancer may rely on regulating the regenerative feedback loop in SCN, which inhibited the proliferation of breast cancer.