Study on testis gene chip of mouse model with syndrome of deficiency of kidney yang.

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 OneArrayTM 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 and controlling life reproduction were explained on the gene level.