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作 者:李伟文[1] 陆松敏[1] 方传勤[1] 刘建仓[1] 柏干荣[1] 程凤[1] 王正国[1]
机构地区:[1]重庆大坪第三军医大学野战外科研究所二室,创伤、烧伤与复合伤国家重点实验室,重庆400042
出 处:《中国现代医学杂志》2012年第24期1-4,共4页China Journal of Modern Medicine
摘 要:目的探讨失血性休克(简称休克)大鼠肠上皮细胞核转录因子mtTFA基因以及核编码线粒体蛋白基因COX Ⅳ和线粒体编码COXⅠ基因表达的改变。以探讨在缺血缺氧性损害中核转录因子mtTFA对线粒体基因组表达的影响。方法采用RT-PCR方法观察休克大鼠肠上皮细胞mtTFA、COXⅠ和COXⅣ基因mRNA量的改变。结果休克早期mtTFA mRNA表达变化不明显,至休克4 h有所增强,到休克5 h下降到休克前水平;休克1 h大鼠肠上皮细胞COXI mRNA表达开始增加,3 h达高峰,后又降低,到休克5 h显著低于休克前水平。休克大鼠肠上皮细胞核基因编码COXⅣmRNA休克3 h略有增高,休克4 h后开始下降,至休克晚期低于休克前水平。结论 mtTFA mRNA表达变化在休克时发生较晚,且升高幅度较小,说明休克时该基因对细胞缺血缺氧性损害的敏感性较低。休克时COX Ⅰ mRNA比COX Ⅳ mRNA上调速度快,维持时间长,说明休克早期线粒体基因表达的改变在细胞缺血缺氧性损伤的保护中起着更重要的作用。[ Objective ] To study changes of expressions of mitochondrial transcription factor A (mtTFA), cytochrome oxidase subunit I (COX I ) and COX IV genes of small epithelia in rats with hemorrhagic shock and to study effects of the nuclear transcription factor on expressions of mitochondrial genome coding the respiratory chain subunits. [ Methods ] The expressions of intestinal mtTFA, COX I and COX IV genes were measured by means of reverse-transcriptional polymerase chain reaction (RT-PCR). [ Results ] The level of mtTFA mRNA had no obvious changes in the early shock. Then it was the highest in shock 4 h and decreased to the pre-shock level in hemorragic shock 5 h group. The expression of COX | mRNA increased gradually in shock lh and the level of COX I mRNA was the highest in shock 3 h. Then it decreased gradually. It lowered significantly in hemorragic shock 5 h group compared with control group (P 〈0.05). The expression of COXIV mRNA increased gradually in shock 3 h. Then it decreased. It lowered markedly in hemorragic shock 5 h group compared with control group(P 〈0.05). [ Conclusion ] The expressions of mtTFA mRNA of intestinal epithelial cells had only slight changes in the late shock stage. It showed that mtTFA was Xower sensitive to ischemia and hypoxia in hemorrhagic shock stage. Relative to changes of expressions of COX IVmRNA, the expressions of COX I mRNA of intestinal epithelial cells in hemorrhagic shock increased quickly and lasted much longer. The changes of mtDNA expression had more important protective action on the damages of cells induced by ischemia-hypoxia in early hemorrhagic shock stage.
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