论文部分内容阅读
目的分析椎动脉型颈椎病(CSA)模型大鼠的肾上腺组织差异基因表达谱变化并探讨肾上腺对CSA的调控机制。方法按照体重将雄性Wistar大鼠随机分为2组:模型组和正常组,用复合造模法建立CSA模型。取模型成功后大鼠的肾上腺组织,提取总RNA,用全基因芯片检测基因表达谱,筛选差异基因,进行基因本体论(GO)、全基因组及代谢途径数据库(KEGG)信号通路分析。结果与正常组比较,模型组差异基因总数为367个(|fold change︱>2,P<0.05),其中表达上调的基因有236个,下调的有131个。富集的GO功能共有2843条,涉及对细胞周期的调节、应力刺激的调节、成纤维细胞增殖的调节及内皮细胞增殖的调节等。参与调节的信号通路共有135条,包括促分裂原活化蛋白激酶(MAPK)信号转导通路、磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号通路、Hedgehog信号通路及Wnt信号通路等。结论肾上腺对CSA的调控主要是通过对血管内皮细胞和血管平滑肌细胞的增殖迁移、黏附分子、成纤维细胞及对刺激的应激反应等实现的。
Objective To analyze the differential gene expression profile of adrenal tissue in rats with vertebral artery type of cervical spondylosis (CSA) and to explore the regulatory mechanism of adrenal on CSA. Methods According to body weight, male Wistar rats were randomly divided into 2 groups: model group and normal group. CSA model was established by compound modeling. Total RNA was extracted from the adrenal tissue of rats after the success of the model. The gene expression profiles were detected by whole-genome microarray, and the differentially expressed genes were screened for gene ontology (GO), whole genome and metabolic pathway database (KEGG) signaling pathways. Results Compared with the normal group, the total number of differential genes in the model group was 367 (| fold change︱> 2, P <0.05). Among them, 236 genes were up-regulated and 131 down-regulated. There are 2,843 GO functions enriched, which are involved in regulation of cell cycle, regulation of stress stimuli, regulation of fibroblast proliferation and regulation of endothelial cell proliferation. A total of 135 signaling pathways are involved, including mitogen-activated protein kinase (MAPK) signaling pathway, phosphatidylinositol 3 kinase / Akt signaling pathway, Hedgehog signaling pathway and Wnt signaling pathway . Conclusion The regulation of adrenal CSA mainly through the proliferation and migration of vascular endothelial cells and vascular smooth muscle cells, adhesion molecules, fibroblasts and stimulation of the response to stress and so on.