中文摘要：

目的：应用基因芯片探讨“劳倦过度、房室不节”肾阳虚小鼠模型睾丸基因改变，从基因水平上探讨肾阳虚证和“肾主生殖”的现代科学机制。方法：连续4周采用雄雌鼠比例1：6同笼喂养和雄鼠每日游泳，建立“劳倦过度、房室不节”肾阳虚小鼠模型。用小鼠全基因组Oligo芯片检测对照组和模型组睾丸基因，以二者荧光信号相对强度比值≥2和≤0．5筛选差异表达基因，查阅北京博奥生物分子注释系统，进行基因功能分类。结果：成功建立“劳倦过度、房室不节”肾阳虚小鼠模型，绘制了对照组与模型组基因表达谱比较的散点图，筛选出差异表达基因，包括上调2425个，下调3080个。其中上调基因前百位中已知基因41个，下调基因前百位中已知基因62个，主要涉及细胞结构／功能、物质/能量代谢、信号转导／传递、炎症／免疫、细胞凋亡、转录／翻译、增殖／分化及细胞周期等。结论：肾阳虚小鼠睾丸基因发生广泛的改变，从基因水平对肾阳虚证的本质及“肾主生殖”的理论做出了一些诠释。

英文摘要：

Objective： To inquire into the testis gene change of mouse model with kidney-yang deficiency induced by overfatigue and excessive sexual life, the modern science mechanism of syndrome of kidney-yang deficiency and kidney controlling reproduction can be revealed on the gene level. Methods： The model of kidney-yang deficiency was established by each male mouse with six female mice keeping in the same cage, and all the male mice were forced to swim for 30-40 minutes everyday lasting for four weeks. The testis genes of mice in control group and model group were detected with Mouse OneArray TM Whole Genome DNA microarray. The differentially expressed genes were screened under the condition of the relative fluorescence intensity ratio of the two groups 〉2 and 〈0.5 and further classified according to gene function by using Molecule Annotation System （MAS） created by CapitalBio Corp. Beijing, China. Results： The mouse model with kidney-yang deficiency was established successfully by the method of overfatigue and excessive sexual life. The scatter plot of gene expression profiles of comparing control group with model group was drawn. Differentially expressed genes were screened, including 2425 up-regulated genes and 3080 down-regulated genes. Among the first one hundred up-regulated genes, 41 genes were known and among the first one hundred down-regulated genes, 62 genes were known. These genes were mainly related to the cellular structure/function, material/energy metabolism, signal transduction/transmission, inflammation/immunization, cell apoptosis, transcription/translation, proliferation/differentiation and cell cycle. Conclusion： The testis gene of kidney-yang deficiency mouse had a wide change. The essence of kidney-yang deficiency syndrome and the theory of the kidney originating arid controlling life reproduction were explained on the gene level.