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目的 应用基因芯片技术分析脂多糖 (LPS)诱导的脓毒症小鼠白细胞基因表达谱变化。方法 5 0只C5 7BL/6J小鼠随机分为脓毒症模型组 (n =2 5 )和正常组 (n =2 5 )。腹腔内注射LPS (15mg/kg)制备小鼠脓毒症模型 ,以肺脏、肝脏、肾脏及胰腺组织病理学变化鉴定模型。应用含 12 4 89条小鼠全长基因的寡核苷酸芯片分别检测脓毒症小鼠和正常小鼠血白细胞的基因表达谱并重复 3次 ,Ratio均数 (RatioAverage,RA) >3及RA <- 3的基因为脓毒症表达差异基因 ,分析表达差异基因与脓毒症之间的关系。结果 脓毒症差异表达基因 5 91中表达上调者为 35 4条 ,下调者为 2 5 7条。脓毒症表达显著增高基因包括 ;转录因子基因 8条、信号转导基因 12条、炎症反应基因 10条、免疫反应基因 4条、黏附分子基因 3条、急性反应蛋白基因 3条、防御反应基因 3条、蛋白酶基因 2条、细胞内吞基因 2条、细胞凋亡基因 4条、代谢酶基因 5条、运输蛋白基因 2条、血管生成基因 1条。脓毒症表达显著降低基因包括 :信号转导基因 1条、黏附分子基因 1条、细胞凋亡基因 1条、防御反应基因 2条、转录因子基因 2条、代谢酶基因 1条。结论 应用芯片技术研究脓毒症小鼠基因表达谱 ,其基因变化的机制模式可能为 :炎症信号激活TPK信号通路及G蛋白介导的
Objective To analyze gene expression profile of leucocytes in sepsis mice induced by lipopolysaccharide (LPS) by gene chip technology. Methods Fifty C5 7BL / 6J mice were randomly divided into sepsis model group (n = 25) and normal group (n = 25). Mice sepsis model was induced by intraperitoneal injection of LPS (15mg / kg), and the pathological changes of lung, liver, kidney and pancreas were identified. The gene expression profile of white blood cells in septic mice and normal mice was detected by oligonucleotide microarrays with 12 4 89 full-length genes and repeated 3 times. Ratio Average (RA)> 3 and The gene of RA - 3 is a differentially expressed gene of sepsis, and the relationship between the differentially expressed genes and sepsis was analyzed. Results There were 35 4 up-regulated genes in 5 91 differentially expressed sepsis and 25 57 down-regulated genes. There were 8 genes of transcription factor, 12 genes of signal transduction, 10 genes of inflammation, 4 genes of immune reaction, 3 genes of adhesion molecule, 3 genes of acute response protein and 3 genes of defense response Three, two protease genes, two endocytosis genes, four apoptosis genes, five metabolic enzyme genes, two transport protein genes and one angiogenesis gene. Sepsis expression significantly reduced genes include: a signal transduction gene, a adhesion molecule gene, a cell apoptosis gene, defense response gene 2, transcription factor gene 2, a metabolic enzyme gene. Conclusion The gene expression pattern of sepsis mice can be studied by using chip technology. The possible mechanism of the gene expression may be that inflammatory signals activate TPK signaling pathway and G protein-mediated