目的探讨薏苡仁不同组分对脾虚水湿不化大鼠空肠基底膜相关转运蛋白和因子基因的影响。方法复制脾虚水湿不化大鼠模型,以事先提取的薏苡仁不同组分对模型进行干预,对空肠进行基因芯片测定;以Quick-GO对差异基因进行富集,对注释到的基底膜组件进行主成分分析(PCA),挖掘最具有代表性的基因。结果 7组样本共注释到差异基因20条,对注释到的差异基因,以主成分分析进行降维,结果发现当提取主成分数目为3时,可以解释资料89.7%的变异,对数据的解释程度良好。对各主成分作用的载荷和得分进行相关性分析发现,在最具有区分价值的第一主成分(PC1)和第二主成分(PC2)上,薏苡仁各治疗组非常接近,说明它们对基底膜相关蛋白的作用类似;而在PC2和第三主成分(PC3)上,它们仍具有各自的特点。进一步探讨其作用靶点,对PC1、PC2和PC3进行归一化后发现,各基因权重不同,权重前10位的为:溶质载体家族22a7(Slc22a7)、碳酸酐酶(Car9)、血管紧张素II受体1b(Agtr1b)、S100钙结合蛋白G(S100g)、水通道蛋白9(Aqp9)、膜突蛋白(Msn)、水通道蛋白3(Aqp3)、溶质载体家族4a1(Slc4a1)、溶质载体家族4a10(Slc4a10)、耳畸蛋白(Otof)。结论薏苡仁能够修复造模刺激导致的小肠损伤,提高模型溶质载体家族(Slc)表达,使小肠募集白细胞的能力得以恢复,这可能是薏苡仁“健脾”作用的体现。薏苡仁能够降低脾虚水湿不化模型的水通道蛋白3(Aqp3)水平,减少水液从肠腔向机体组织的吸收,是薏苡仁“利湿”作用的体现。 Objective To investigate the effects of different components of Coix seed on the transporter and related genes of jejunum basement membrane in rats with spleen deficiency and water dampness. METHODS: The model of spleen-asthenia-dampness-dampness was duplicated, and the different components of pre-extracted Coix seed were used to intervene the model to determine the jejunum gene chip. The differential gene was enriched by Quick-GO. The principal component analysis (PCA), mining the most representative genes. Results A total of 20 differential genes were annotated in the 7 groups of samples, and the differentially expressed genes were reduced by principal component analysis. As a result, it was found that when the number of principal components extracted was 3, 89.7% of the data could be interpreted as explanatory data A good degree Correlation analysis of the loads acting on the principal components and the scores found that the coix seed treatment groups were very close on the most discriminative first principal component (PC1) and second principal component (PC2) Membrane associated proteins function similarly; whereas, on PC2 and the third principal component (PC3), they still have their own characteristics. To further explore its role as a target, PC1, PC2 and PC3 were normalized and found that the weight of each gene was different. The top ten weights were as follows: family of solute carrier 22a7 (Slc22a7), carbonic anhydrase (Car9), angiotensin II receptor 1b (Agtr1b), S100 calcium binding protein G (S100g), aquaporin 9 (Aqp9), membrane protein (Msn), aquaporin 3 (Aqp3), solute carrier family 4a1 (Slc4a1) Family 4a10 (Slc4a10), Otof protein. Conclusion Coix seed can repair small intestine damage induced by modeling and increase the expression of Slc in the model so as to restore the ability of the small intestine to raise white blood cells. This may be the result of Coix seed. Coix seed can reduce the level of aquaporin 3 (Aqp3) in the spleen-qi stagnation model and reduce the absorption of water from the intestinal lumen into the body tissues, which is the effect of Coix Seed “dampness ”.