中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2009年
1期
44-47,后插二
,共5页
李志军%王东强%胡顺鹏%王小飞%何英%张照健
李誌軍%王東彊%鬍順鵬%王小飛%何英%張照健
리지군%왕동강%호순붕%왕소비%하영%장조건
基因芯片%菌毒炎并治%脓毒症%鼠%肝%动物模型
基因芯片%菌毒炎併治%膿毒癥%鼠%肝%動物模型
기인심편%균독염병치%농독증%서%간%동물모형
gene chip%"Jun Du Yan Bingzhi"%sepsis%rat%liver%animal model
目的 应用基因芯片技术探讨菌毒炎并治对脓毒症大鼠基因的改变,以期从基因水平上探讨其药物作用机制.方法 将90只大鼠随机分为正常对照组、模型组、菌毒炎组,每组30只;采用盲肠结扎穿孔术(CLP)复制脓毒症模型.菌毒炎组于制模后腹腔注射泰能0.18 g/kg、血必净注射液10 ml/kg、中药复方凉膈散煎剂15 ml/kg(药物浓度6 kg/L)灌胃,每日2次;正常对照组和模型组腹腔给予生理盐水10 ml/kg.观察大鼠存活时间及48 h和72 h的存活率;应用BiostarR-40 s芯片检测模型组/正常对照组,菌毒炎组/模型组鼠肝基因,并以Cy3和Cy5二者荧光信号相对强度比值≥2.0或≤0.5筛选差异显著基因,通过美国国立生物技术信息中心(NCBI)数据库查询基因功能并加以分类.结果 菌毒炎组大鼠48 h和72 h存活率明显高于模型组(83.3%比30.0%,76.7%比17.7%,P均<0.01),模型组/正常对照组共筛选出305个差异基因,其中上调159个、已知基因109个,下调基因146个、已知基因89个;菌毒炎组/模型组共筛选出500个差异基因,其中上调292个、已知基因175个,下调基因208个、已知基因148个.模型组/正常对照组上调而菌毒炎组/模型组下调的已知基因共有48个,模型组/正常对照组下调而菌毒炎组/模型组上调的已知基因共有63个.结论 菌毒炎并治可显著降低脓毒症大鼠48 h和72 h死亡率;通过调控免疫反应、炎症、信号转导、转录调节、细胞周期、细胞凋亡、新陈代谢、蛋白翻译/加工/修饰/降解、细胞分化/增殖/生长等相关基因,能促使脓毒症大鼠多系统功能恢复正常.
目的 應用基因芯片技術探討菌毒炎併治對膿毒癥大鼠基因的改變,以期從基因水平上探討其藥物作用機製.方法 將90隻大鼠隨機分為正常對照組、模型組、菌毒炎組,每組30隻;採用盲腸結扎穿孔術(CLP)複製膿毒癥模型.菌毒炎組于製模後腹腔註射泰能0.18 g/kg、血必淨註射液10 ml/kg、中藥複方涼膈散煎劑15 ml/kg(藥物濃度6 kg/L)灌胃,每日2次;正常對照組和模型組腹腔給予生理鹽水10 ml/kg.觀察大鼠存活時間及48 h和72 h的存活率;應用BiostarR-40 s芯片檢測模型組/正常對照組,菌毒炎組/模型組鼠肝基因,併以Cy3和Cy5二者熒光信號相對彊度比值≥2.0或≤0.5篩選差異顯著基因,通過美國國立生物技術信息中心(NCBI)數據庫查詢基因功能併加以分類.結果 菌毒炎組大鼠48 h和72 h存活率明顯高于模型組(83.3%比30.0%,76.7%比17.7%,P均<0.01),模型組/正常對照組共篩選齣305箇差異基因,其中上調159箇、已知基因109箇,下調基因146箇、已知基因89箇;菌毒炎組/模型組共篩選齣500箇差異基因,其中上調292箇、已知基因175箇,下調基因208箇、已知基因148箇.模型組/正常對照組上調而菌毒炎組/模型組下調的已知基因共有48箇,模型組/正常對照組下調而菌毒炎組/模型組上調的已知基因共有63箇.結論 菌毒炎併治可顯著降低膿毒癥大鼠48 h和72 h死亡率;通過調控免疫反應、炎癥、信號轉導、轉錄調節、細胞週期、細胞凋亡、新陳代謝、蛋白翻譯/加工/脩飾/降解、細胞分化/增殖/生長等相關基因,能促使膿毒癥大鼠多繫統功能恢複正常.
목적 응용기인심편기술탐토균독염병치대농독증대서기인적개변,이기종기인수평상탐토기약물작용궤제.방법 장90지대서수궤분위정상대조조、모형조、균독염조,매조30지;채용맹장결찰천공술(CLP)복제농독증모형.균독염조우제모후복강주사태능0.18 g/kg、혈필정주사액10 ml/kg、중약복방량격산전제15 ml/kg(약물농도6 kg/L)관위,매일2차;정상대조조화모형조복강급여생리염수10 ml/kg.관찰대서존활시간급48 h화72 h적존활솔;응용BiostarR-40 s심편검측모형조/정상대조조,균독염조/모형조서간기인,병이Cy3화Cy5이자형광신호상대강도비치≥2.0혹≤0.5사선차이현저기인,통과미국국립생물기술신식중심(NCBI)수거고사순기인공능병가이분류.결과 균독염조대서48 h화72 h존활솔명현고우모형조(83.3%비30.0%,76.7%비17.7%,P균<0.01),모형조/정상대조조공사선출305개차이기인,기중상조159개、이지기인109개,하조기인146개、이지기인89개;균독염조/모형조공사선출500개차이기인,기중상조292개、이지기인175개,하조기인208개、이지기인148개.모형조/정상대조조상조이균독염조/모형조하조적이지기인공유48개,모형조/정상대조조하조이균독염조/모형조상조적이지기인공유63개.결론 균독염병치가현저강저농독증대서48 h화72 h사망솔;통과조공면역반응、염증、신호전도、전록조절、세포주기、세포조망、신진대사、단백번역/가공/수식/강해、세포분화/증식/생장등상관기인,능촉사농독증대서다계통공능회복정상.
Objective To study the effect of"Jun Du Yan Bingzhi"on genic change in liver of a sepsis rat model by gene chip technique,in order to study the mechanism of the action of the drug on the gene level.Methods Ninety rats were randomly divided into normal control group,model group and"Jun Du Yan Bingzhi"group,with 30 rats in each group.Sepsis was reproduced by cecal ligation and puncture(CLP) method.In"Jun Du Yan Bingzhi rt group the rats were treated with intraperitoncal injection of imipenem/cilastatin(0.18 g/kg),Xuebijing injection(10 ml/kg)and gavage of"Liangge San"(15 ml/kg).In the control group and model group intraperitoncal physiological saline(10 ml/kg)was given.Survival time,and 48-hour and 72-hour survival rates of every group were observed,and changes in liver genes were examined with BiostarR-40 s chip.The ratio of Cy3/Cy5≥2.0 or≤0.5 was used to screen differential genes,and NCBI database was used to identity the function of differential genes.Results The 48-hour and 72-hour survival rate of"Jun Du Yan Bingzhi"group was significantly higher than that of model group(83.3%vs.30.0%,76.7%vs.17.7%,both P<0.01),305 differential genes were found in model/crotrol groups,with up-regulation in 159,down-regulation in 146,500 differential genes were found in"Jun Du Yan Bingzhi"group/model group,with up-regulation in 292,down-regulation in 208,model group/control group up-regulation and"Jun Du Yan Bingzhi"group/model group down-regulation were 48,model group/control group down-regulation and " Jun Du Yan Bingzhi"group/model group up-regulation were 63.Conclusion"Jun Du Yan Bingzhi"can degrade the 48-hour and 72-hour death rate of sepsis rat,through control immunization related,inflammation,signal transduction、transcription regulation,cell cycle,apoptosis,substance metabolism,translation/processing/modify/degradation of protein,differentiation/proliferation/growth of cell related gene,promote multisystem function of sepsis rat to recover normal.