Objective To study the changes in whole genome expression profiles of the tongue in a rat model of Qi-stagnation and blood stasis by gene chip microarray as well as the biological processes and pathways related to the differentially expressed genes, and to provide scientific evidence for studies of the related theories and drug therapies of blood stasis syndrome. Methods The rat model of Qi-stagnation and blood stasis was established by high-fat diet combined with chronic unpredictable mild stress (CUMS). Changes of the whole genome expression profiles of the tongue in normal rats and model rats and the involved pathways were analyzed by gene chip microarray. Results Compared with the normal rats, the rats with Qi-stagnation and blood stasis showed 277 differentially-expressed genes, including 68 up-regulated and 209 down-regulated genes. Gene ontology (GO) and pathway analysis showed that the syndrome of Qi-stagnation and blood stasis is related to biological processes such as inflammation, lipid metabolism and immune responses, as well as the alterations in 7 pathways including the complement and coagulation cascade pathway, the PPAR signaling pathway, and the pathway of xenobiotic metabolism by cytochrome P450. Conclusions The differentially-expressed genes, which are involved in CYP450 and complement and coagulation cascade pathway and PPAR signal pathway, may be related to the pathogenesis of blood stasis syndrome, and provide evidence for studies of blood stasis and related drug development.