不同气虚证小鼠甲状腺G蛋白通路及相关基因转录特征

Characteristics of G Protein Signaling Pathway and Related Gene Expression in Thyroid of Mice with Different Qi-Deficiency Syndromes

目的:观察不同气虚证小鼠甲状腺G蛋白信号通路及功能激素基因表达的特征。方法:采用小鼠计量化四诊和辨证方法,以及GeneChip Mouse Exon 1.0 ST Array等技术,观察正常小鼠、肿瘤气虚证荷瘤小鼠甲状腺G蛋白信号通路及相关基因表达特征。结果:不同气虚小鼠垂体TSH与甲状腺TSH受体(TSHR)表达量均增加,但正常气虚证小鼠甲状腺G蛋白通路的腺苷酸环化酶(AC)和蛋白激酶A(PKA)未见相应的表达量增加;而肿瘤气虚证小鼠则相应增加、活跃,发生响应,Ras基因亦如是。结论:正常气虚小鼠甲状腺G蛋白通路中大多基因表达不活跃可能是其部分物质基础,而荷瘤小鼠气虚证系因实致虚,因此表现与正常气虚证不同,即甲状腺尚处于代偿状态。

This study aimed to analyze characteristics thyroid of mice with different qi-deficiency syndromes of G protein signaling pathway and related gene expression in （QDS）. Quantitative four diagnosis, syndrome differentiation methods, and Affymetrix GeneChip Mouse Exon 1.0 ST Array were used. Thyroid gene expression of normal mice and tumor mice with QDS were detected. Genes of G protein signaling pathway and related hormones in gene chips were selected. And then, characteristics of gene expression were analyzed. The results showed that the expression of thyroid stimulating hormone （TSH） and TSHR were increased in thyroid of QDS mice. And the adenylate cyclase （AC） and protein kinase A （PKA） in G protein signaling pathway were increased in thyroid of QDS tumor mice, but not in the normal QDS mice. The Ras genes also follow the same trend. It is concluded that most inactive genes may be the material base of QDS among normal mice. However, QDS among tumor mice was different from normal QDS mice. Since the QDS in tumor mice is caused by excess, and the thyroid was in compensation condition.