中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2009年
7期
702-706
,共5页
许会彬%黄灵芝%郑伟%李晓峰%王字玲%周虹
許會彬%黃靈芝%鄭偉%李曉峰%王字玲%週虹
허회빈%황령지%정위%리효봉%왕자령%주홍
失血性休克%DNA芯片%基因表达%肝脏
失血性休剋%DNA芯片%基因錶達%肝髒
실혈성휴극%DNA심편%기인표체%간장
Hemorrhagic shock%DNA chip%Gene expression%liver
目的 应用基因芯片技术分析失血性休克组(hemorrhage shock,HS)及对照组(sham hemorrhage shock,SHAM)大鼠肝脏差异基因表达谱,从分子水平探讨HS可能的病理生理机制.方法 20只雄性Wistar大鼠随机分成SHAM组和HS模型组,每组10只.采用5705点的大鼠寡核苷酸芯片分别检测HS大鼠及SHAM大鼠肝脏基因表达谱,重复三次并计算Ratio(R)均数,R≥2时表示基因上调;R≤0.5时表示基因下调.对差异表达基因的功能进行分析并用RT-PCR对其中9条基因的表达水平进行验证.结果 在大鼠5705条靶基因中,初步筛选出86条差异表达基因,其中上调基因72条,下调基因14条.根据基因的生物学功能,差异表达基因主要为:物质转运相关基因、转录调节相关基因、信号转导相关基因、应激反应相关基因、代谢相关基因、发育相关基因、细胞黏附相关基因等.结论 HS的发生是由多基因参与的复杂调控过程;芯片试验结果对进一步探讨HS可能的病理生理机制以及为探求HS治疗的新靶点提供了依据.
目的 應用基因芯片技術分析失血性休剋組(hemorrhage shock,HS)及對照組(sham hemorrhage shock,SHAM)大鼠肝髒差異基因錶達譜,從分子水平探討HS可能的病理生理機製.方法 20隻雄性Wistar大鼠隨機分成SHAM組和HS模型組,每組10隻.採用5705點的大鼠寡覈苷痠芯片分彆檢測HS大鼠及SHAM大鼠肝髒基因錶達譜,重複三次併計算Ratio(R)均數,R≥2時錶示基因上調;R≤0.5時錶示基因下調.對差異錶達基因的功能進行分析併用RT-PCR對其中9條基因的錶達水平進行驗證.結果 在大鼠5705條靶基因中,初步篩選齣86條差異錶達基因,其中上調基因72條,下調基因14條.根據基因的生物學功能,差異錶達基因主要為:物質轉運相關基因、轉錄調節相關基因、信號轉導相關基因、應激反應相關基因、代謝相關基因、髮育相關基因、細胞黏附相關基因等.結論 HS的髮生是由多基因參與的複雜調控過程;芯片試驗結果對進一步探討HS可能的病理生理機製以及為探求HS治療的新靶點提供瞭依據.
목적 응용기인심편기술분석실혈성휴극조(hemorrhage shock,HS)급대조조(sham hemorrhage shock,SHAM)대서간장차이기인표체보,종분자수평탐토HS가능적병리생리궤제.방법 20지웅성Wistar대서수궤분성SHAM조화HS모형조,매조10지.채용5705점적대서과핵감산심편분별검측HS대서급SHAM대서간장기인표체보,중복삼차병계산Ratio(R)균수,R≥2시표시기인상조;R≤0.5시표시기인하조.대차이표체기인적공능진행분석병용RT-PCR대기중9조기인적표체수평진행험증.결과 재대서5705조파기인중,초보사선출86조차이표체기인,기중상조기인72조,하조기인14조.근거기인적생물학공능,차이표체기인주요위:물질전운상관기인、전록조절상관기인、신호전도상관기인、응격반응상관기인、대사상관기인、발육상관기인、세포점부상관기인등.결론 HS적발생시유다기인삼여적복잡조공과정;심편시험결과대진일보탐토HS가능적병리생리궤제이급위탐구HS치료적신파점제공료의거.
Objective To analyze the differential gene expression profiling of liver in rats subjected to hemorrhagic shock(HS) and sham hemorrhage shock(SHAM) by gene chip technology, thus to evaluate the possible molecular pathogenesis of HS. Method 20 male Wistar rats were randomly divided into a SHAM group and a HS group, with 10 rats in each group. Hepatic gene expression profiles were detected by oligonucleotide microarrays of 5705 mouse genes in two groups for three times. Genes with ratio(R) > 2 were identified as up-regulated and R < 0.5 were identified as down-regulated. Biological function of differentially expressed genes was analyzed and 9 genes were selected to undergo semi-quantitative RT-PCR. Results Among the total 5705 probes detected,86 genes showed differential expression in HS group comparison with SHAM group. The expression levels of 72 genes were up-regulated while those of 14 genes were down-regulated significantly. Differentially expressed genes were classified according to their biological function: transport genes, transcription regulator genes, signaling genes, response to stress genes, metabolic genes, development genes and cell adhesion genes. Conclusions cDNA microarray is an efficient and high-throughout method to survey gene expression profiles in HS.The variation of those gene expressions might be a potential pathogenic mechanism for HS that may offer a novel target for further study of therapeutic strategies of HS.