中文摘要：

目的：研究脾虚水湿不化大鼠脾虚湿阻的分子机制。方法：20只Wistar大鼠随机分为模型组和正常对照组,每组10只。高脂低蛋白加负重力竭游泳复合因素诱导6周,建立脾虚水湿不化大鼠模型。Agilent全基因组表达谱芯片检测大鼠十二指肠组织基因表达谱变化,筛选差异基因,基于基因本体数据库（GO）进行基因功能分类,基于《京都基因与基因组百科全书（KEGG）》数据库进行信号通路分析,实时荧光定量PCR验证部分基因Tff2和Trpm6表达。结果：与正常对照组比,模型大鼠筛选出1275个差异表达基因,上调660个,下调615个。GO分析结果显示差异基因生物学过程主要包括跨膜转运、免疫应答、铁离子稳态等,分子功能主要包括水通道活性、磷脂酶D活性、受体活性、氧化还原酶活性等,细胞组分包括微绒毛、刷状缘膜等。信号通路主要包括矿物质吸收、补体级联反应、细胞因子-细胞因子相互作用、钙离子信号通路、甘氨酸、丝氨酸、苏氨酸代谢通路。结论：模型大鼠十二指肠组织参与消化吸收、水及离子代谢、免疫功能的基因出现异常,其脾虚湿阻的机制涉及矿物质吸收、钙离子信号通路、补体激活通路及甘氨酸、丝氨酸、苏氨酸代谢等。

英文摘要：

Objective： To explore the molecular mechanism of＂dampness stagnancy due to spleen deficiency＂in the model rats by studying the whole gene expression profile of the duodenum. Methods： Twenty Wistar rats were randomly divided into the model group and normal control group and Agilent rat gene expression microarray was used to identify changes in gene expression of rats＇ duodenum. The differentially expressed genes（ DEGS） were screened out and analyzed based on Gene Ontology（ GO） and Kyoto Encyclopedia of genes and genomes（ KEGG）. Quantitative real-time PCR was used to validate expression ratios of the DEGS obtained from the microarray hybridization. Results： Compared with the control group,1275 genes were differentially expressed,in which 660 genes were up-regulated and 615 were down-regulated. According to the enrichment analysis of GO analysis,biological process involved in transportation,immune response,iron ion homeostasis,molecular function involved in water channel activity,phospholipase D activity,receptor activity,oxidoreductase activity,and cellular component involved in brush border,collagen,microvillus. The pathways of DEGS according to KEGG analysis involved calcium signaling pathway,cytokine-cytokine receptor interaction,mineral absorption,complement and coagulation cascades,glycine,serine and threonine metabolism. Conclusion： The expression of genes related to digestion,absorption and immune in rats with dampness stagnancy due to spleen deficiency was changed. The mechanisms of water stagnancy due to spleen deficiency might be related to calcium signaling pathway,cytokine-cytokine receptor interaction,mineral absorption,complement and coagulation cascades,glycine,serine and threonine metabolism.