肝部分切除+定容失血性休克大鼠肝脏cDNA表达谱芯片结果分析 |
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引用本文: | 易伟,钱琤,张育瑆,俞晓军,胡志前,方国恩. 肝部分切除+定容失血性休克大鼠肝脏cDNA表达谱芯片结果分析[J]. 浙江创伤外科, 2013, 18(3): 289-293 |
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作者姓名: | 易伟 钱琤 张育瑆 俞晓军 胡志前 方国恩 |
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作者单位: | 1. 上海第二军医大学附属长征医院, 上海,200003 2. 上海第二军医大学附属长海医院 |
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摘 要: | 目的 利用cDNA表达谱芯片分析肝部分切除+定容失血性休克前和休克后24小时大鼠肝脏差异基因,并初步分析差异基因信号通路和网络调控. 方法 11只大鼠接受肝左外叶切除和2.5ml/100g体重定容失血性休克,选其中3只存活大鼠麻醉后失血前切除肝左外叶(A组),对于存活24小时的大鼠再次取肝脏(B组)行cDNA表达谱芯片(含21793个基因)分析.对差异基因行Pathway、Go、Network分析.使用RT-PCR对两组中基因Aldh1a1、Aldh1a7、Aoc3、Cyp26a1、Hdc1、Ephx2和Beta-actin进行分析,验证cDNA芯片的准确性. 结果 4只大鼠存活24小时,表达谱芯片筛查出两组差异表达下调基因634个,表达上调基因513个.差异基因涉及主要信号通路包括胆固醇代谢、细胞外刺激反应、甾醇代谢、激素刺激反应、甾体类激素刺激反应、类固醇代谢、内源性刺激反应、氧化还原反应、有机物质反应、脂肪酸代谢.结论 氧化还原和脂代谢信号通路在创伤失血性休克病理过程中起重要作用.
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关 键 词: | 创伤 失血性休克 大鼠 信号通路 基因芯片 调控网络 |
Use of cDNA microarray profiling to analyze the differential expressed genes in the liver of rats with hepatectomy and fixed volume hem- orrhagic shock |
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Affiliation: | YI Wei, QIAN Zheng, ZHANG Yuxing, et al. (Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.) |
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Abstract: | Objective Use of cDNA microarray profiling to analyze the differential expressed genes in the liver of rats before and 24 h after partial hepatectomy + fixed volume hemorrhagic shock, and analyze the pathway and regulation network in the genes screened. Methods 9 SD rats undertook left lobular hepatectomy and 2.5ml/100g body weight fixed volume hemorrhagic shock. Of those who survived over 24 h, the livers before hemorrhage (group A) and 24 h after hemorrhage (group B) were used in the microarray chip analysis. The pathway, gene ontology, network were also analyzed. The expression of Aldhlal, AldhlaT, Aoc3, Cyp26al, Hdcl, Ephx2 and Beta-actin genes were detected by RT-PCR to testified the accura- cy of the data from microarray chip. Results 4/9 rats survived over 24 h,634 genes down regulated and 513 genes up regulated in group B when compared with group A. The following pathway analysis revealed that the differential genes involved mainly in metabolic pathways, fatty acid metabolism, drug metabolism-cytochrome P450, PPAR signaling pathway, metabolism of xenobiotics by cytochrome P450, terpenoid backbone biosyn- thesis, retinol metabolism, biosynthesis of unsaturated fatty acids, linoleic acid metabolism, glycolysis/gluconeogenesis. Conclusion The genes in- volved in the oxidation reduction and metabolism of lipid were crucial in the recovery from severe traumatic hemorrhagic shock. |
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Keywords: | Trauma Hemorrhagic shock Signaling pathway Microarray profiling Rrgulatory Networks |
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