中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2008年
7期
515-521
,共7页
陈蕾%王世鑫%刘萍%魏茂提%栾大伟%何瑞波%涂植光
陳蕾%王世鑫%劉萍%魏茂提%欒大偉%何瑞波%塗植光
진뢰%왕세흠%류평%위무제%란대위%하서파%도식광
矽肺%寡核苷酸序列分析%大鼠%肺
矽肺%寡覈苷痠序列分析%大鼠%肺
석폐%과핵감산서렬분석%대서%폐
Silicosis%Oligonucleotide array sequence analysis%Rat%Lung
目的 研究染矽尘大鼠早期肺组织与正常肺组织的差异基因表达谱.方法 应用气管暴露法建立雄性Wistar大鼠染矽尘模型和对照组,每组3只,应用Illumina激光共聚焦光纤微珠基因芯片技术,研究建模后14 d时的大鼠肺组织差异基因表达谱,并采用DAVID生物信息学分析工具,进行Fisher精确概率检验,对差异基因的基因功能和生物学通路进行富集统计学分析.结果 检测出的有效基因共22 107个,筛选出染矽尘组与对照组的差异基因共1567个,其中上调基因为765个,下调基因为802个.在KEGG生物学通路数据库中,共406个差异基因获得注释,上调基因为204个,其中11个生物学通路相关基因显著上调;下调的基因有202个,其中3个生物学通路相关基因显著下调.Real-time PCR实验验证了血红素加氧酶1(HMOXl)、超氧化物歧化酶2(SOD2)基因上调的趋势和基因芯片结果是一致的.结论 本次实验筛选出了染矽尘早期大鼠肺组织差异基因,提示矽尘致肺纤维化过程中可能存在相互作用的基因簇.
目的 研究染矽塵大鼠早期肺組織與正常肺組織的差異基因錶達譜.方法 應用氣管暴露法建立雄性Wistar大鼠染矽塵模型和對照組,每組3隻,應用Illumina激光共聚焦光纖微珠基因芯片技術,研究建模後14 d時的大鼠肺組織差異基因錶達譜,併採用DAVID生物信息學分析工具,進行Fisher精確概率檢驗,對差異基因的基因功能和生物學通路進行富集統計學分析.結果 檢測齣的有效基因共22 107箇,篩選齣染矽塵組與對照組的差異基因共1567箇,其中上調基因為765箇,下調基因為802箇.在KEGG生物學通路數據庫中,共406箇差異基因穫得註釋,上調基因為204箇,其中11箇生物學通路相關基因顯著上調;下調的基因有202箇,其中3箇生物學通路相關基因顯著下調.Real-time PCR實驗驗證瞭血紅素加氧酶1(HMOXl)、超氧化物歧化酶2(SOD2)基因上調的趨勢和基因芯片結果是一緻的.結論 本次實驗篩選齣瞭染矽塵早期大鼠肺組織差異基因,提示矽塵緻肺纖維化過程中可能存在相互作用的基因簇.
목적 연구염석진대서조기폐조직여정상폐조직적차이기인표체보.방법 응용기관폭로법건립웅성Wistar대서염석진모형화대조조,매조3지,응용Illumina격광공취초광섬미주기인심편기술,연구건모후14 d시적대서폐조직차이기인표체보,병채용DAVID생물신식학분석공구,진행Fisher정학개솔검험,대차이기인적기인공능화생물학통로진행부집통계학분석.결과 검측출적유효기인공22 107개,사선출염석진조여대조조적차이기인공1567개,기중상조기인위765개,하조기인위802개.재KEGG생물학통로수거고중,공406개차이기인획득주석,상조기인위204개,기중11개생물학통로상관기인현저상조;하조적기인유202개,기중3개생물학통로상관기인현저하조.Real-time PCR실험험증료혈홍소가양매1(HMOXl)、초양화물기화매2(SOD2)기인상조적추세화기인심편결과시일치적.결론 본차실험사선출료염석진조기대서폐조직차이기인,제시석진치폐섬유화과정중가능존재상호작용적기인족.
Objective To study the differential gene expression profiling of rats exposed to silica using the normal rats as contr01. Methods Animal models were established using intratrachea injection of the lung and 22 107 genes were screened in the differential expression profiling of silicosis by using oligonucleotide bead array. Differential expression profiling data were analyzed by using DAVID bioinformation software. Results Totally 1567 differentially expressed genes were identified in lungs of silica exposed rats including 765 up-regulated genes and 802 down-regulated genes as compared to the normal controls. Among 406 annotated genes in KEGG pathways.204 genes and 11 pathways were up- regulated as well as 202 genes and 3 pathways were down- regulated in silica exposed rats. Conclusion A1l 1567 genes are involved in the formation of silicosis. The differential gene expression profile of silicosis describes the general changes in the gene expressions in silicosis at transcriptional level. Further analysis of the identified genes might help reveal the molecular mechanism of pulmonary fibrosis induced by silica.