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作 者:刘小美[1] 方肇勤[1] 潘志强[1] 卢文丽[1] 管冬元[1] 粱超[1] 吴中华[1]
出 处:《北京中医药大学学报》2011年第6期396-401,共6页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家科技重大专项资助项目(No.2009ZX09502-018);上海市教委学科建设资助项目
摘 要:目的分析同病异证荷瘤小鼠垂体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、及GeneChip Mouse Exon 1.0 ST Array等技术,观察正常小鼠、早期邪毒壅盛证和气虚证荷瘤小鼠垂体G蛋白信号通路及功能激素相关基因表达特征。结果邪毒证和气虚证小鼠垂体G蛋白信号通路中的PP2B、Calm1所含基因的表达趋势基本一致,但在绝对表达量上,邪毒证均较气虚证低;另外气虚证垂体G蛋白信号通路中的ras基因均比较活跃,而在邪毒证中有高有低,特别是Kras基因,邪毒证的表达量只有气虚证的55%。与正常组比较,邪毒证小鼠垂体Lhb、Tshb表达升高,Fshb、Cga和Prl表达降低,而Pomc和Gh的表达基本不变;而这些基因在气虚证小鼠垂体中全部上调。结论肿瘤发生后,垂体G蛋白信号通路及功能激素基因表达水平总体呈上调趋势,而同期的邪毒壅盛证荷瘤小鼠较气虚证小鼠偏弱,这可能与邪毒壅盛证荷瘤小鼠预后差有关。Objective To analyse the gene expression characteristics of pituitary signal pathway of G protein and functional hormones in the tumor-bearing mice with different syndromes Methods The characteristics of gene expressions related to pituitary signal pathway same disease. G protein and functional hormones were observed in normal mice (normal group), tumor-bearing mice with syndrome of pathogenic toxin stagnation at early stage (pathogenic toxin group) and tumor-bearing deficiency syndrome (qi deficiency group) by applying measurementized four diagnosis mice with qi and syndrome differentiation methods and the technology of GeneChip Mouse Exon 1.0 ST Array. Results The expressive trends of PP2B and Calml genes of signal pathway of pituitary G protein were not different between the pathogenic toxin group and qi deficiency group, but the absolute expression was lower in the pathogenic toxin group than that in the qi deficiency group. The ras genes of signal pathway of pituitary G protein were active in the qi deficiency group but not stable in the pathogenic toxin group, especially Kras gene and its expression was in the pathogenic toxin group only 55% of that in the qi deficiency group. Compared with the normal group, the expressions of pituitary Lhb and Tshb increased, expressions of Fshb, Cga and Prl decreased and expressions of Pomc and Gh had no changes in the pathogenic group, while all these gene expressions were up-regulated in the qi deficiency group. Conclusion The gene expressions related to pituitary signal pathway of G protein and functional hormones show a upward trend after tumor generation, but which are lower in the tumor-bearing mice with the syndrome of pathogenic toxin stagnation than those in the tumor-bearing mice with the qi deficiency syndrome. It may be related to that the tumor-bearing mice with the syndrome of pathogenic toxin stagnation have poorer prognosis.
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