气滞血瘀证大鼠舌部基因表达谱变化初探

目的采用基因芯片技术研究气滞血瘀证模型大鼠舌部全基因表达谱的变化以及差异基因涉及的生物过程和通路,以期为研究血瘀证相关理论和药物治疗提供科学依据。方法采用高脂饲料复合慢性不可预知刺激复制气滞血瘀动物模型,利用基因芯片技术分析正常大鼠与模型大鼠舌中全基因表达谱的变化以及所涉及通路。结果气滞血瘀证大鼠与正常大鼠比较,结果显示差异表达基因有277个,其中上调基因68个,下调基因209个。GO和Pathway分析结果显示气滞血瘀证分别与炎症、脂代谢、免疫反应等生物过程以及补体与凝血级联通路、PPAR信号通路、细胞色素P450异物代谢通路等7条通路的改变有关。结论 CYP450以及补体与凝血级联通路、PPAR信号通路中的差异基因可能涉及血瘀证的发病机制,为血瘀证以及相关药物的研究提供依据。

Preliminary study on changes in genome expression profiles of the tongue in rats with Qi-stagnation and blood stasis

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.